Brainscape's Knowledge GenomeTM

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


See full index

Year 1: LSS 2 > Alimentary System > Flashcards

Alimentary System Flashcards

1
Q

What are the organs of the gastrointestinal tract?

A

Mouth, oesophagus, stomach, small intestine, liver, biliary system, pancreas, large intestine

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

What does the colon consist of?

A

Caecum, appendix, ascending colon, hepatic flexure, transverse colon, splenic flexure, descending flexure, sigmoid colon

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

What are the components of the burden of disease?

A

Patient burden, Health costs, Morbidity, Mortality, Incidence and prevalence

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

What are the general symptoms of GI diseases?

A

Anorexia, Weight Loss, Anaemia

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

What are the symptoms of diseases in the upper GI tract?

A

Haematemesis, Malena, Vomiting, Nausea, Dysphagia, Odynophagia, Heart burn, Acid regurgitation, Chest pain, Belching, Epigastric Pain

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

What are the symptoms of disease of the liver and biliary system?

A

Right upper quadrant pain, biliary colic, Icterus (jaundice), Pruritus (dark urine), Cholestasis (pale stool) Ascities (abdominal distension)

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

What are the symptoms of disease of the Mid GI tract and pancreas?

A

Abdominal pain, diarrhoea, Steatorrhoea, Distension

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

What are the symptoms of disease of the lower GI tract?

A

Abdominal pain, diarrhoea, bleeding, constipation, incontinence (inappropriate passing of urine)

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

What are general signs of GI disease?

A

Cachexia, Obesity, Lymphadenopathy, Anaemia, Jaundice

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

What are the signs of GI disease in the hands?

A

Koilinychia (thin, brittle, concave nails.
Leuconychia (white discolouration of nails)
Clubbing
Tachycardia
Tremor
Dupytrens contracture (flexion deformity of fingers)

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

What are the signs of GI disease in the abdomen?

A

Organ enlargement
Mass
Tenderness
Distension

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

What are the signs of GI disease in the anus and rectum?

A

Haemorrhoids (enlargement of blood filled spongy cushions in the anus)
Fistula (abnormal communication between two organs)
Fissure (break in skin lining anal canal)
Rectal masses
Proctitis (inflammation of the rectum)

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

General statistics about GI disease

A 
1/8 Hospital Admissions
Responsible for 12% Deaths in the UK
1/4 Main operations
Drug prescriptions>£4 billion
5% adults suffer chronic illness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Major GI Diseases

A

Worldwide- Malnutrition, enteric infections, gastric cancer, viral hepatitis

UK- dyspepsia, liver disease, colon cancer

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

What are the three areas of the small intestine?

A

Jejunum, Ileum, Duodenum

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

What are the roles of the areas of the small intestine?

A

Absorption of blood, nutrients and water from the lumen to the blood

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

What is the size of the small intestine and its components?

A

Small intestine: 6m long, 3.5 cm diameter
Duodenum: 25 cm
Jejunum: 2.5m
Ileum: 3.75 m

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

What is the function of the mesentery?

A

It surrounds the small intestine and is folded and has a large blood supply to support the metabolic functions of the cell as well as aid absorption

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

Describe the digestive epithelium

A

It lies on the external muscular wall (consisting of circular and longitudinal muscles) and has an internal folded mucosa which are covered in villi (around 1mm long) and have invaginations called crypts of leiberkuhn)

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

Describe the intestinal epithelium

A

Simple epithelium (1 cell thick) consists of columnar absorptive cells (enterocytes) and are interspersed with goblet and enteroendocrine cells)

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

What are the properties of villi?

A

Motile
Large Blood Supply
Good Lymphatic Drainage
Innervation from submucosal plexus

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

What do crypts of Lieberkun consist of?

A

Paneth Cells

Stem Cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the most abundant cell in the small intestine?

A

Enterocytes

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

What are the properties of enterocytes?

A

Tall columnar
Apical microvilli
Basal nuclei

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

What is the life span of an enterocyte?

A

1-6 days

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

What is the use of tight junctions between cells?

A

Intercellular communication

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

What is the size of the microvilli?

A

0.5-1.5 micrometres

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

Which membrane of enterocytes do the microvilli overly?

A

Apical membrane

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

Where does the glycocalyx reside?

A

On the apical membrane of the enterocytes and is a rich carbohydrate layer

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

What is the function of the glycocalyx?

A

Protects microvilli and enterocytes from digestion from digestive enzymes.
Provides environment for digestion to take place

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

How does the glycocalyx provide an environment for absorption?

A

Traps a layer of mucous and water known as the ‘unstirred layer’ which contains many enzymes and regulates the rate of absorption from the lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

To what extent does the villi, microvilli and mucosal folds increase the surface area of the small intestine?

A

By 500x. From 0.4 m 2 to 200 m2

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

What is the second most abundant epithelial cell type in the small intestine?

A

Goblet cell

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

What is the reason for the characteristic shape of the goblet cell?

A

Mucous filled granules accumulate at the apical end

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

How does the position of granules in the goblet cell aid secretion?

A

Secretion is unidirectional

Products go into lumen, NOT blood

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

What is mucous?

A

A large glycoprotein that facilitates the movement of digested material through the bowel

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

Describe the abundance of goblet cells in the small intestine

A

Fewer in duodenum compared to colon. Number increases along length of small intestine.

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

What type of cell are enteroendocrine cells?

A

Columnar epithelial cells found mainly in the lower part of the crypts
Hormone secreting cells (chromaffin cells)

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

Where are paneth cells found?

A

In the base of the crypts

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

What do paneth cells contains?

A

Acidophilic granules which contain lyzozomes (protect cell from bacterial pathogens), glycoproteins and zinc

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

How do pluripotent cells replace goblet cells and enterocytes?

A

Divide by mitosis and migrate to villus tip

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

How do pluripotent cells die?

A

Senescence (shed off into lumen and digested)- escalator of epithelial migration, first line of defence against GI diseases

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

What can effect the escalator of epithelial migration?

A

Radiation

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

How can the cholera toxin lead to dehydration and death?

A

Results in prolonged opening of chloride channels in small intestine so more water goes into lumen resulting in water diarrhoea

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

How is a person with cholera treated?

A

Oral rehydration therapy

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

Why is treatment for the bacteria not required?

A

The body will expel the bacteria and enterotoxin due to rapid turnover of the cells

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

Describe the differences in appearance of the different areas of the small intestine

A

Duodenum- Brunners glands which have alkaline secretions
Jejunum- taller and thinner plicae circulars (valves of Kerckring)
Ileum- Peyers patches (like large intestine)

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

What is the cause of the frilly interior of the jejunum?

A

The circular folds of the mucosa

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

How do peyers Patches protect the body?

A

Prime the immune system and prevent bacteria from migrating into the small intestine from the colon due to its position

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

What are the functions of small intestine motility?

A

Neutralise stomach chime and mix food with digestive enzymes
Facilitate contact between intestine and intestinal mucosa
Propel intestinal contents along the alimentary tract

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

What are the processes of small intestine motility?

A

Segmentation
Peristalsis
Migrating Motor Complex

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

What is segmentation

A

Frequent stationary contractions of circular muscles at intervals to mix contents of lumen

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

What is peristalsis

A

Propels chime towards colon due to sequential contraction of smooth muscle, waves are about 10cm apart

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

What is the migrating motor complex recognised as

A

Rumbling stomach

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

What is the migrating motor complex?

A

Waves of smooth muscle contractions which during fasting which prevents the movement of colonic bacteria into the ileum and clears the intestine of residual food.
Waves begin in colon, and when they reach terminal ileum they start in the duodenum

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

What are the four mechanism of absorption?

A

Passive diffusion
Facilitated diffusion
Primary active transport
Secondary active transport

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

What is the source of energy for primary and secondary active transport

A

Primary active transport: hydrolysis of ATP

Secondary active transport: electrochemical gradient

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

How much of ingested calories is owed to carbohydrates?

A

50%

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

Where does most digestion of carbohydrates occur?

A

Small intestine, primarily on the unstirred layer

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

What happens in the intestine in response to a meal for carbohydrate digestion?

A

Pancreatic alpha-amylase is secreted into the duodenum which requires Cl- and an alkaline environment which is provided by the Brunner’s glands

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

How are the different sugar molecules absorbed?

A

Glucose & Galactose- Secondary active transport on carrier protein SGLT-1 on apical membrane
Fructose- Facilitated diffusion on carrier protein GLUT-5 on apical membrane

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

How do sugar molecules exit the carrier protein

A

GLUT-2 on basolateral membrane

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

Where does digestion of proteins begin?

A

In stomach due to pepsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How are pancreatic proteases involved in digestion

A

They are secreted into the small intestine (trypsinogen) then converted on the duodenal brush border into trypsin by the action of enterokinase.
Trypsin carries on digestion and activates other proteases.

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

How are proteins broken down?

A

After being broken down into large polypeptides, brush border peptidases break them down further into di/tri peptides and free amino acids

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

How are the products of protein digestion absorbed?

A

Di/tri peptides: facilitated diffusion and secondary active transport
Free amino acids: carrier proteins followed by breakdown into amino acids by cytoplasmic peptidases before they cross the basolateral membrane

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

What are the stages of digestion of lipids?

A

Secretion of bile and lipase’s
Emulsification
Enzymatic hydrolysis of ester linkages
Solubilisation of lipolytic products in micelles

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

What is the purpose of emulsification?

A

Lipids are poorly soluble therefore the surface area of fat for digestion is increased

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

Describe the structure of bile salts

A

Amphipathic with steroid nucleus
Bile acid Hydrophobic face
Hydrophilic face with OH groups on carboxyl/sulfonic acid
Hydrophobic face dissolves in fat and hydrophilic face dissolves in water

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

What is the function of bile salts?

A

Facilitate emulsification into suspension of lipid droplets which allows pancreatic lipase to split triglycerides into two fatty acids and a monoglyceride.

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

What prevents bile salts from displacing lipase from the micelle?

A

Pancreatic lipase forms complexes with colipase

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

What is the function of phospholipase A2

A

hydrolyses fatty acids at the 2 position of phospholipids which forms lyso-phospholipids and free fatty acids

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

What is the function of pancreatic cholesterol esterase

A

Hydrolyses cholesterol esters to free cholesterol and fatty acids

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

How are lipid digestion products absorbed

A

Micelles can be transported across the unstirred layer and present monoglycerides and fatty acids to the brush border. Bile salts are absorbed in ileum but lipid aborption is complete by mid-jejunum.

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

How are bile salts recylced

A

Transported back to liver via enterohepatic circulation

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

What does lipid metabolism involve

A

Re-synthesis of triglycerides in enterocytes

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

What are the two pathways of lipid metabolism

A 
Monoglyceride acylation (major)
Phosphatidic acid (minor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is monoglyceride acylation?

A

Fatty acids bind to the apical membrane and fatty acid binding proteins transfer them to the smooth endoplasmic reticulum where they are esterified to triglycerides

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

What is the phosphatidic acid pathway?

A

Triglycerides are synthesised from CoA fatty acid and alpha- phosphoglycerate

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

What are chylomicrons?

A 
After triglyceride synthesis, lipoproteins are synthesised as an emulsion consisting of :- 
80-90% triglycerides 
8-9% phospholipids 
2% cholesterol
2% proteins and trace carbohydrates

They are transported to basolateral membrane of golgi and secreted by exocytosis and enter lacteals due to large size

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

What prevents back flow of bacteria from colon to ileum

A

Ileocaecal sphincter

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

What causes undernutrition

A

Inadequate consumption, poor absorption, excessive loss of nutrients

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

Why is BMI less relevant in undernourished patients?

A

Severely undernourished people may have fluid imbalance which will affect weight

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

What are surrogate measurements for undernourished patients?

A

Arm circumference and arm skin-folds

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

What are nutrient requirements?

A

The amount needed to be consumed by an individual in order to maintain optimal health and function and avoid deficiency

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

Which hormones regulate feeding

A

PYY- GI hormone with anorexic effect
Ghrelin- stomach and pancreatic hormone with orexigenic effect
Leptin- Long term effects, released from adipocytes with anorexic effect

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

What are the effects of leptin

A

Cessation of menstrual cycles

Obesity leads to leptin resistance

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

What is BERIBERI?

A

thiamine deficiency

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

What is thiamine

A

Occurs as free thiamine and various phosphorylated forms (monophosphate, triphosphate and pyrophosphate)
Needed for the release and utilisation of energy from food and nerve function (found on neurone membranes)
Found in unrefined cereals and fresh foods

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

What are the properties of BERI BERI

A

Ailment of nervous system
Lethargy and fatigue
Effects cardiovascular, nervous, muscular and GI systems
Found in people with diet of polished white rice
Alcoholics
Post-gastric bypass patients

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

PELLAGRA

A

Niacin deficiency

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

Why is niacin important

A

Nicotinamide is derivative of niacin and forms coenzymes NAD and NADP
Niacin coenzymes are needed

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

What are the signs of undernutrition?

A 
Muscle wasting
Weight loss 
Loss of subcutaneous fat (loose skin on extremities)
Glossitis 
Har loss 
Infections
Peripheral oedema (no cardiac disease)
Listless
Poor wound healing
Recurrent pulmonary infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is the passive response to energy restriction/starvation to decrease resting metabolic rate?

A 
Decrease insulin
Decrease thyroxine and T3
Release glucagon
Release growth hormone
Substrate mobilisation of free fatty acid and amino acid leading to weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What is the active response to reduced energy flux?

A

Decreased SNS activity
Increase catecholamine production
Decreased metabolic flux and energy expenditure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are the effects of short and long fasts?

A

Short fasts: Loss of glycogen and associated water from liver and gut weight
Long fasts: Further gut and liver weight and muscle weight and fat loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Normal metabolic rate

A

25-30kcal/kg/d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What does the pancreatic bud form?

A

The dorsal and ventral mesenteries of the foregut in function with the midgut
Dorsal bud expands on left to form head neck body and tail
Duodenum rotates and forms C-shape, ventral bud forms rest of head and uncinate process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Where are islets of Langerhans most prevalent in the pancreas

A

Tail

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

How does pancreatic juice reach the duodenum?

A

Main and accessory pancreatic ducts which fuse with the common bile duct to enter the duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What forms of imaging is used to assess pancreatic tumours and disease?

A

MRI- tumours

Angiography- disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What do pancreatic juices consist of?

A

Digestive enzymes and HC03-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

How are endocrine cells formed?

A

From the branching duct system (tail of pancreas) then lose contact and differentiate further

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

How is the major pancreatic duct formed?

A

Connective tissue between exocrine acinar cells and endocrine islet cells with columnar epithelium and minor pancreatic duct fuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What are the components of pancreatic juice

A

Low volume, viscous rich in digestive enzymes secreted by acinar cells
High volume, water solution rich in HC03 secreted by centroacinar and duct cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What are the differences between acinar and duct cells?

A

Acinar cells are large with apical secretory granules (containing inactive precursors protecting the cells from auto digestion)
Duct cells are small with few granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What is the concentration and pH of bicarbonate secretion

A

120 mM

7.5-8 pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is the mechanism of secretion

A

Separation of H+ and HC03-
Transport of H+ and HC03- out of the duct cell
Mainenance of Na+ gradient
Movement of K+ into blood and Cl- into duct cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

How is the NA+ gradient maintained

A

Na/K pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What are zymogens?

A

Pro enzymes which store lipases, amylases and proteases and protect the acini and ducts from auto digestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Why can acute pancreatitis lead to auto-digestion

A

Blockage can lead to overload of zymogen protection

112
Q

How does the pancreas ensure protein digestion only occurs in duodenum

A

Secrets trypsin inhibitor

113
Q

How does enterokinase activate tryspin

A

Cleaves trysinogen between valine and isoleucine

114
Q

What is an anti-obesity drug

A

ORLISTAT- pancreatic lipase inhibitor

115
Q

What are the phases of pancreatic secretion

A

Cephalic
Gastric
Intestinal

116
Q

How is the cephalic phase initiated

A

Pancreatic secretion enters before food enters the duodenum via the vagal reflex in response to taste and smell. Cholinergic synapses resulting in enzymes.

117
Q

What initiates the intestinal phase

A

When acid chime enters the duodenum from the stomach, the duodenal mucosa secretes secretin and CCK into the blood

118
Q

What is secretin and CCK

A

Secretin is formed in response to acidic pH and stimulates bicarbonate secretion- involves cAMP
CCk is formed in response to fats/proteins and stimulated enzyme production. Involves calcium ions and PLC via vagus reflex

119
Q

What ends the cephalic phase

A

The meal being eaten

120
Q

What ends the intestinal phase

A

The absorption of fats/proteins therefore the removal of the stimulus for CCK production

121
Q

What are the roles of bile?

A

Cholesterol homeostasis
Dietary lipid/vitamin absorption
Removal of xenobiotic/drugs/waste products

122
Q

Which GI Pathogens affects the mouth?

A

Oral Candidiasis

123
Q

Give examples of gastric pathogens

A

Hectobacter pylori, e.coli, noravirus, cholera

124
Q

What innate GI Defence mechanisms are there?

A

Gastric acid

Oral commensal flora,

125
Q

What innate GI Defence mechanisms are there?

A 
Gastric acid
Oral commensal flora
Peristalsis
Mucous from goblet cells
Proteases
Brush border
126
Q

What is rich in MALT

A

Oral cavity

Tongue, palatine, lingual and pharyngeal tonsils

127
Q

What are the differences between organised and unorganised GALT

A

Not organised: lamina propria lymphocytes and intra-epithelial lymphocytes
Organised: cryptopatches, Peyers patches, isolates lymphoid follicles, mesenteric lymph nodes

128
Q

Within the gut mucosa, what is dome epithelium?

A

Areas with no mucosa epithelium, but rather M cells, act as portal of entry for antigens to be transferred to lymphocytes, macrophages and dendritic cells

129
Q

How is IgA transported from submucosa to the lumen?

A

Transyctosis

130
Q

What are the groups of CD4 cells

A

Th1- cellular immunity
Th2- humoral immunity
Treg- immunoregulatory function
Th17- inflammation and autoimmunity

131
Q

What are the symptoms of Crohns disease

A

Structuring
Ulceration
Inflammation

132
Q

What are the symptoms of Crohns disease

A

Structuring
Ulceration
Inflammation

133
Q

Where does the liver lie?

A

The right upper quadrant, superior border at 5th costal cartilage

134
Q

How to percuss liver

A

Percuss chest inferiorly, percuss abdomen superiorly and dull area is liver

135
Q

What separates the two lobes of the liver

A

Falciform ligament

136
Q

Why is the gallbladder not palpable

A

Lies inferior to arch of liver, if palpable then an enlargement is indicated

137
Q

How much of cardiac output is received by the liver

A

25%

138
Q

Explain the dual supply of the liver

A

20% is artery blood from left and right branches of hepatic artery and is oxygen rich.
80% is venous blood from gut from the hepatic portal vein and is nutrient rich

139
Q

Why is the liver protected from acute ischemia if an embolus is present.

A

It has a direct and indirect blood supply

140
Q

What are the function of the liver

A 
Synthesise bile pigments
Breakdown over-dated RBC 
Secrete bile into duodenum 
Secrete bile pigments into bile
Site of insulin dependent glycogen storage
141
Q

Where does the liver arise from?

A

Septum transversum

142
Q

Where may the common bile duct join the pancreatic duct?

A

The ampulla

143
Q

What can be used to view the biliary tree?

A

ERCP

144
Q

What are the resident liver macrophages?

A

Kupffer cells which reside in the space

145
Q

How could hepatic stellate cells cause cirrhosis?

A

They contain vitamin a which if due to toxic insult may deposit fibrous tissue and lead to fibrosis

146
Q

What is the Space of Disse

A

Space between hepatocyte and associated sinusoid epithelium

147
Q

Why is the endothelium fenestrated?

A

To allow movement of substances

148
Q

What are the characteristics of a diseased liver?

A

Endothelium lose fenestrae, stellate cells deposit into space of Disse, Kupffer cells unregulated and produce free radicals which cause further damage and hepatocytes lose microvilli

149
Q

What are common causes of acute pancreatitis?

A

Alcoholism and cholelithiasis

150
Q

What is classified obese with regards to waist circumference?

A

Men> 102 Women >88

151
Q

What is classified obese with regards to hypertension?

A

bp> 135/80

152
Q

What is classified obese with regards to HDL count?

A

Men> 1 Women>1.3

153
Q

What is classified obese with regards to Fasting glucose?

A

> 6mmol

154
Q

Explain gastric bypass surgery

A

Stops calories coming into contact with duodenum so reduces fat absorption

155
Q

How can acute liver failure be subdivided

A

Hyperacute : Less than 7 days between jaundice and encephalopathy
Acute: Between 1 to 4 weeks
Subacute: Between 5 and 28 weeks

156
Q

What are the causes of acute liver failure

A

Hyperacute: paracetamol, Hep A Hep B
Acute: Hep A, B, E idiosyncratic drug toxicity
Subacute: Non A Non B heptatitis

157
Q

What are the causes of chronic liver disease?

A

Alcoholism
Chronic viral hep b and c
Sclerosing cholangitis
Primary biliary cirrhosis

158
Q

What are the clinical features of chronic liver disease

A

Portal hypertension
Oesophageal varices
Ascites

159
Q

What are the plexi in the GIT

A

Meyenteric
Submucosal
Minor

160
Q

What is the submucosal plexus continuous with

A

Duodenum and large intestine

161
Q

What is the purpose of the submucosal plexus

A

Senses environment within lumen and then controls gut secretion, gut endocrine and epithelial function and blood flow

162
Q

Where is gastrin synthesised

A

Antrum and upper small intestine

163
Q

What inhibits gastrin secretion

A

pH

164
Q

Where is secretin synthesised

A

S cells of upper duodenum and jejunum

165
Q

What stimulates secretin

A

pH of less than 4.5 in duodenum

166
Q

Where is Gastric Inhibtory Peptide synthesised

A

K cells of duonedum and jejunum

167
Q

What does GIP stimulate

A

Secretin

168
Q

Where is PYY synthesised

A

L cells in ileum, rectum, colon

169
Q

When is PYY stimulated?

A

After eating

170
Q

What are the main functions of the liver

A

Digestion
Energy metabolism
Detoxification

171
Q

Where does the biliary system drain into?

A

From ductules into right and left hepatic ducts into the common hepatic duct, which joins the cystic duct to drain into the common bile duct

172
Q

What is gluconeogenesis?

A

Process of forming glucose from non-carbohydrate sources

173
Q

What is the cori cycle?

A

Glucose is broken down anaerobically by muscles into lactate which is then converted into glucose in the liver

174
Q

How can glucose be formed from triglycerides or deamination?

A

Triglycerides- glycerol- glucose

Alanine- pyruvate- glucose

175
Q

How much of plasma proteins are synthesised by the liver?

A

90%

176
Q

What is transamination?

A

The production of non essential amino acids from an alpha-keto precursor. Involved an amino group from one amino acid and a ketone group from another.

177
Q

What is deamination?

A

Conversion of an amino acid into its corresponding leto acid by removing the amine group as ammonia and replacing it with a ketone group

178
Q

What is urea?

A

NH2C(O)NH2

179
Q

How is urea formed?

A

Liver converts ammonia into urea using carbon dioxide which is then excreted in the urine

180
Q

What are the the properties of urea?

A

Soluble
Metabolically inert
Non toxic

181
Q

How can fats be used as an energy source?

A

Fatty acids can be converted into acetyl coA which can then enter the TCA cycle

182
Q

What do lipoproteins consist of?

A

Triglycerides, cholesterol core, phospholipid and protein coat

183
Q

What are the various types of lipoproteins

A 
VDL= lots of triglycerides 
IDL= intermediate density lipoproteins
LDL= Lots of cholesterol and phospholipids
HDL= High protein coat
184
Q

Which is the most dense lipoprotein

A

HDL- the lower the density, the larger the diameter

185
Q

Why is CETP of interest to drug companies?

A

It shuttles cholesterol of HDL’s to LDL’s. High HDL:LDL ratio is significant in the prevention of atherosclerosis.

186
Q

What is a phospholipid?

A

Fatty acid, phosphoric acid and nitrogenous base

187
Q

What is cholesterol?

A

Sterol nucleus synthesised from acetyl coa and dietary intake

188
Q

Where does secretion of bile occur?

A

Through canniculi between adjacent hepatocytes into the biliary system

189
Q

How are cholic and chenodeoxycholic acids formed?

A

Oxidation of cholesterol. Carboxyl and hydroxyl groups are then added to make the acids soluble

190
Q

What are the products of conjugated primary bile acids?

A

taurcholic and glycocholic acid

191
Q

How are secondary bile salts formed?

A

Primary bile salts are deconjugated and dehydroxylated and converted with GI bacteria

192
Q

What dothe hydrophobic and hydrophilic faces of bile salts consist of?

A

Hydrophobic- nuceus and methyl groups

Hydrophilic- hydroxyl and carboxyl groups

193
Q

Where is the ampulla of Vater located?

A

2nd part of duodenum

194
Q

How is bile released?

A

Released into the ampulla of cater during digestion. Some is released during the cephalic and gastric stages as a result of the vagal nerve and gastrin secretion. However most bile is released during the intestinal phase as a result of CCK secretion causing the gallbladder to contract and relaxation of the sphincter of Oddi

195
Q

What happens to bile salts when they enter hepatic circulation?

A

Bile salts are actively absorbed in the terminal ileum. They are de-hydroxylated and de-conjugated with colonic bacteria to make them more lipid soluble
They are sent back to the liver via the hepatic portal vein.
Hepatocytes remove all bile salts from the hepatic portal vein and they a re-conjugated and re-hydroxylated

196
Q

How many times during a meal is the bile salt pool secreted?

A

Twice

197
Q

Why is lecithin useful for excess cholesterol

A

Allows more cholesterol into micelles

198
Q

How is bilirubin produced

A

Porphirin group of harm is broken down to bilirubin in the spleen. In the liver it is conjugated to glucoronic acid and excreted in the bile

199
Q

Which fat soluble vitamins does the liver store?

A

A, D, E, K. Stores last for 6-12 months except the small store of Vit K which poses a problem as Vit K is needed for blood clotting

200
Q

What does the Liver store

A

Vitamins A,D,E,K
Iron as ferritin, available for erythropoeisis
Vitamin B12- lack leads to pernicious anaemia and nerve demyelation
Fat and glycogen

201
Q

How is the liver protected from pathogens

A

Kupffer cells which are resident macrophages in liver sinusoids destroy pathogens which enter enterohepatic circulation from the lumen of the gut
This will prevent the pathogen from entering the rest of the body

202
Q

How is vitamin D formed

A

UV light is required to convert cholesterol into a Vitamin D precursor.
The precursor then requires double hydroxylation to convert it into Vitamin D.
The first hydroxylation occurs in the liver and the second occurs in the kidneys.

203
Q

What are the layers of the gut wall?

A

Mucosa
Submucosa
Muscularis
Serous/adventitia

204
Q

How does food reach the pharynx?

A

Tongue pushes food into pharynx from mouth which is under neural control

205
Q

Where does the pharynx become the oesophagus?

A

C5- ending at t10

206
Q

How is the oesophagus protected from wear and tear?

A 
Stratified squamous epithelium 
Non keratinising- therefore is moist 
Mucous secreting glands 
Protective layers
2 sphincters- pressure in oesophagus is less than the atmosphere so they prevent the backtracking of food
207
Q

What causes the upper oesophageal sphincter to open?

A

The swallowing centre in the medulla under parasympathetic control via the vagus nerve

208
Q

What happens if the bolus of food gets stuck?

A

A second wave of peristalsis is initiated

209
Q

What is the mechanism of the lower sphincter?

A

Resides at the Z-line of gastro-oesophageal junction
Not a sphincter as such
Due to pressure difference between stomach and oesophagus
Contraction of the diaphragm
When stomach expands, it compressed the Z-line

210
Q

What is heartburn

A

Because the lower sphincter is not foolproof, acid from stomach can go up into the oesophagus

211
Q

Why may the lower sphincter not be efficient in pregnancy?

A

Stomach is forced upwards, and sphincter is forced into thorax. Pressure difference is lost as is the contractility of the diaphragm.

212
Q

What is the function of the stomach?

A

To break down the bolus of food and hold food and release it periodically into duodenum and kill bacteria/parasites.

213
Q

What are the secretions of the stomach

A

Cardia and pyloris- mucous
Body and fundus- mucous, acid, pepsinogen
Antrum- gastrin

214
Q

What do the parietal and and endocrine cells in the stomach produce?

A

Parietal- HCl

Endocrine- gastrin

215
Q

What is the pH of the epithelium and lumen?

A

Epithelium- 6-7 (neutralised by bicarbonate ions trapped in the mucus)
Lumen- 1-2

216
Q

What is a chief cell?

A

Cell that produces pepsinogen

Well adapted for protein synthesis, contains large amounts of RER, Golgi and secretory granules

217
Q

What is the appearance of the parietal cell in the resting state?

A

Lots of mitochondria, concentrating the H+ ions is a very active process requiring much ATP
Internal reservoirs and canaliculi

218
Q

What is the appearance of the parietal cell in the active state?

A

Tubular vesicles fuse with canaliculi which fuse to form reservoirs that extend to the apical membrane.
On the basolateral membrane there is an Na/K pump. K+ diffuses across lumen.
H+ is actively exchange into the cell for K+.
Bicarbonate ions are exchanged for Cl- ion which diffuse into the cell
Cl- and H+ join to form HCl

219
Q

How is pepsin formed

A

Pepsinogen has an internalised active site which is protected
Acid of the stomach exposes the active site. Hcl reacts with pepsinogen to form pepsin.
Via positive feedback, Pepsin catalyses its own production.
Pepsin is a protease

220
Q

What are the functions of gastrin

A

Produced in antrum of stomach
Stimulates histamine release from chromaffin cells of lamina propria
Together, these two things cause the increase of acid in the stomach.
Negative feedback- more acidic stomach gets, the more gastrin secretion is inhibited

221
Q

How does a protein rich meal lessen gastrin inhibition?

A

Protein acts as a good buffer for acid

222
Q

How does Ach prepare for arrival of food?

A

Stimulates parietal cells to produce acid and chromaffin cells to release histamine indirectly

223
Q

What causes gastrin and Ach to be released in the gastric phase?

A

Food enters stomach and distension stimulates stretch receptors.
Contents stimulates chemoreceptors leading to a local enteric response

224
Q

What effect does the intestinal phase have on the production of gastrin?

A

Inhibitory

Food enters small intestine, more alkaline environment is required.

225
Q

What does the large intestine consist of?

A

Caecum, appendix, rectum, colon, anal canal

226
Q

What are the dimensions of the colon?

A

1.5 m long

6cm diameter

227
Q

What are the main functions of the colon?

A

Reabsorption of electrolytes/water and elimination of undigested food/waste

228
Q

What are the structural features of the colon?

A

Appendicies Epiploicae
Taeni coli
Haustra
Solitary nodules

229
Q

What are taeni coli?

A

3 longitudinal bands running along the length of the colon

Needed for large intestine motility

230
Q

Where does most electrolyte water reabsorption occur?

A

Proximial colon

231
Q

What is the mechanism of reabsorption?

A

Na+ and Cl- ions are absorbed by exchange mechanisms and ion channel.
Water follows by osmosis.
K+ diffuses in passively

232
Q

How much water can the large intestine absorb?

A

Up to 4.5 l - above this diarrhoea will occur

233
Q

What is the rectum?

A

The dilated distal portion of the alimentary canal

234
Q

How is the rectum distinguished from the colon?

A

Has transverse folds in the submucosa and no taeni coli in muscular is externa

235
Q

How many goblet cells are in the large intestine in comparison to the small intestine?

A

More goblet cells in large intestine, predominantly in the crypts. Required for mucous secretion to move solid contents of intestine.
Acetylcholine stimulate goblet cells secretion

236
Q

What cell type is present in the small intestine but not the large intestine?

A

Paneth cells

237
Q

What is the difference between the glycocalyx of the small intestine and large intestine?

A

It does not contain digestive enzymes in the large intestine

238
Q

What is haustra

A

When the longitudinal layers of taeni coli penetrate the circular layers of muscle at intervals.
They contracts individually

239
Q

Why is motility important?

A

Promotes the reabsorption of electrolytes and water

240
Q

Which type of food promotes mass movement in the large intestine?

A

Food with a lot of fibre

241
Q

Describe the parasympathetic innervation of the large intestine

A

Vagus nerve innervates the ascending colon and most of the transverse colon
Pelvic nerve innervates more distally

242
Q

Describe the sympathetic innervation of the large intestine

A

Thoracocolumnar outlflow

243
Q

What is the external anal sphincter controlled by?

A

Somatic motor fibres in the pudendal nerve

244
Q

What is the defecation reflex controlled by?

A

Sacral spinal chord

Includes reflex on voluntary actions

245
Q

Describe defecation

A

Filling of the rectum causes a reflex in response to distension of the walls
Pressure receptors send signals via the meyenteric plexus to start peristaltic waves in the descending colon, sigmoid colon and rectum.
The internal anal sphincter is inhibited.
The external anal spinster is under voluntary control.
The urger can be resisted and feeling can subside.

246
Q

What is the social part of the rectum

A

The last few cm which can distinguish between solid, liquid and gas

247
Q

How much faeces is produced in a day

A

150 g

2/3 water

248
Q

What gives the odour to faeces

A

Bacterial fermentation

249
Q

What solids are contain in faeces?

A

Bacteria, bile pigments, salts, cellulose and cell debris

250
Q

What is microbiome

A

The symbiotic relationship that mammals have with their gut microbial community

251
Q

What is the role of the flora?

A

Synthesise and secrete vitamins
Prevent bacteria from colonising by competing for areas of nutrients
Produce cross reactive antibodies
Antagonise bacteria by producing substances to inhibit or kill
Stimulate production of certain tissue such as caecum and lympathic

252
Q

What are the types of flora?

A

Bacteroides- non sporeforming, anaerobic, gram negative

Bifidobacteria- non sporeforming, gram positive, lactic acid bacteria

253
Q

Which type of flora is the most prevalent?

A

Bacteroides

254
Q

Which type of flora is implicated in the initiation of colitis and colon cancer?

A

Bacteroides

255
Q

Which type of flora is thought to prevent the colonisation of certain pathogens?

A

Bifidobacteria

256
Q

What is a normal weight of bowel movement?

A

200g a day

257
Q

What are two presenting features of malabsorption?

A

Diarrhoea/ Steatorrhoea
Weight loss
Growth failure

258
Q

What would you assess for malnutrition?

A

Loss of fat
Muscle wasting
Ascites
Oedema

259
Q

What causes maldigestion?

A

Reduced gastric tissue/secretions
Reduced pancreatic tissue
Reduced bile secretion
Reduced brush border enzymes

260
Q

What causes malabsorption?

A

Loss of enterocyte function
Pre & post mucosal effects
Single gene disorders

261
Q

What is Coeliac disease?

A

Inflammatory disease of the upper intestine due to gluten ingestion in susceptible individuals

262
Q

What does coeliac disease present as?

A

Subtotal villus atrophy

263
Q

What is the main gene involved in coeliac disease?

A

HLA-DQ2

264
Q

What is ethanol insoluble in?

A

Fats and oil

265
Q

How is ethanol metabolised?

A

Ethanol converted into acetaldehyde by alcohol dehydrogenase
Acetaldehyde converted into carbon dioxide and water by acetaldehyde dehydrogenase

266
Q

Why can Asians not metabolise alcohol efficiently?

A

They are deficient in aldehyde dehydrogenase

267
Q

What alternative pathways are present for metabolising alcohol?

A

CYP2E1 and catalase

268
Q

How can tolerance be explained?

A

The more alcohol consumed, the more CYP2E1 that can be produced

269
Q

What problems can CYP2E1 cause?

A

Free radicals are a bi-product of this pathway and can lead to inflammation

270
Q

What are the long term effects of alcohol?

A 
Pancreatic damage
Myocardial damage
Enhanced toxicity
Fatty liver 
Ongoing liver damage
Carcinogenesis
271
Q

What is steatosis

A

fatty liver

272
Q

What is steatohepatitis

A

Fatty liver with inflammation

273
Q

What are the consequences of steatosis and steatohepatitis

A

Fibrosis

274
Q

How can alcoholism lead to hepatocyte fibrosis

A

Chronic inflammation can lead to hepatic stellate cells within the space of Disse to turn into fibroblasts. These will lay down collagen fibres that will condense into fibrous bands

275
Q

What are the types of diarrhoea

A

Secretory
Osmotic
Inflammatory
Hypermotility

Year 1: LSS 2 (3 decks)

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