13. Gut flux and motility Flashcards

1
Q

primary peristaltic wave

A

forces the bolus down the esophagus and into the stomach

wave lasts about 8–9 seconds

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2
Q

secondary peristaltic wave

A

In the event that the bolus gets stuck

a secondary peristaltic wave occurs

forces the bolus further down the esophagus

waves continues until the bolus enters the stomach

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3
Q

What part of the brain controls the process of peristalsis?

A

medulla oblongata

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4
Q

5 Functions of the Fundus (Proximal stomach)

A

1) Gastro duodenal flow
2) Intragastric pressure
3) Temporary storage
4) Tonic motor activity
3) Stimulates propulsion

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5
Q

What % of body weight does the pancreas represent

A

0.1%

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6
Q

How may enzymes does the pancreas release?

A

15 digestive enzymes

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7
Q

4 Functions of the small bowel

A

Lymphoid tissue
Absorption
Immune function
Digestion

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8
Q

Where is Lymphoid Tissue concentrated

A

Terminal ileum

Tonsils

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9
Q

3 Functions of the large bowel

A

Salvage of water and electrolytes

Absorption of undigested carbohydrates

Secretion of mucus

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10
Q

How is the small bowel adapted for Immune function?

A

MALT (GALT) made up of B and T cells

Peyer’s patches (discrete clusters of immune cells)

Secretory IgA

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11
Q

How is the small bowel adapted for Absorption

A

Microvilli = large S.A

Motility = allows contact of contents with absorptive surfaces

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12
Q

Where is majority of iron absorbed?

A

Duodenum

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13
Q

Where is majority of folate absorbed?

A

Jejunum

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14
Q

Where is majority of B12 absorbed?

A

Ileum

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15
Q

Where does majority of water absorption occur?

A

ascending and transverse colon

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16
Q

What 4 factors determine Fluid Absorption?

A

Luminal Osmolarity
Motility
Mucosal Integrity
S.A

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17
Q

Oral intake of fluid a day

A

2L

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18
Q

Biliary fluid entering a day

A

0.5L

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19
Q

Pancreatic fluid entering a day

A

1L

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20
Q

Intestinal fluid entering a day

A

1L

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21
Q

Gastric fluid entering a day

A

2.5L

22
Q

Salivary fluid entering a day

A

1.5L

23
Q

Fluid reabsorbed in to small intestine a day

A

7L

24
Q

Fluid reabsorbed in to large intestine a day

A

1.4L

25
Q

Treatment of FH (Familial Hypercholesterolaemia)

A

statins

26
Q

Classification of hyperlipidaemias

Fredrickson/WHO (1970)

A

Type I Increased CMs
Type IIa Increased LDL
Type IIb Increased LDL and VLDL
Type III Increased Remnants and IDL
Type IV Increased VLDL
Type V Increased Chylomicrons and VLDL

27
Q

Familial Type III Hyperlipidaemia

A

Mechanism: defective remnant clearance

Prevalence: 1 in 5000

Inheritance: autosomal recessive

Physical Signs: striate palmar and tuberoeruptive xanthomata

28
Q

Familial Hypercholesterolaemia

A

Mechanism: LDL Receptor defect

Prevalence: 1 in 500

Inheritance: Autosomal dominant

Physical Signs: Tendon Xanthomata, corneal arcus

29
Q

Familial Combined Hyperlipidaemia

A

Mechanism: overproduction of VLDL and apoB

Physical Signs: variable, Xanthelasmata

Prevalence: 1 in 100

Inheritance: variable, some autosomal dominant

30
Q

Familial Hypertriglyceridaemia

A

Physical Signs: prone to pancreatitis and diabetes mellitus

Prevalence: 1 in 300

Inheritance: variable

31
Q

post MI treatment

A

atorvastatin 80mg

32
Q

Statins mode of action

A

inhibit cholesterol synthesis

increase hepatic LDL receptor activity

33
Q

Fibrates mode of action

A

activate PPAR alpha

↑ LPL activity

↑ biliary cholesterol secretion

34
Q

Bile Acid Binding Resins mode of action

A

divert cholesterol into bile acid synthesis

interrupt enterohepatic circulation of bile acids

↑ hepatic LDL receptor activity

35
Q

Cholesterol Absorption Inhibitors mode of action

A

reduce enterohepatic cholesterol recycling

36
Q

PCSK9 Inhibitors mode of action

A

antibodies to PCSK9

37
Q

advantages of statins

A

potent

mostly well tolerated

single (nightly) dose

38
Q

disadvantages of statins

A

muscle toxicity

hepatic toxicity

may aggravate liver disorder

39
Q

advantages of fibrates

A

potent

mostly well tolerated

quite cheap

40
Q

disadvantages of fibrates

A

muscle toxicity

↑ incidence of gallstones

potential for toxic interactions

41
Q

ezetimibe

A

used to treat hypercholesterolaemia

used for patients intolerant to statins

42
Q

management of abdominal pain

A

NG tube
Oxygen therapy
Proton pump inhibitors
IV fluids

43
Q

Likelihood of colorectal cancer in Ascending colon

A

30%

44
Q

Colorectal cancer

Right Sided Lesion

A

Present later

Less likely to cause diarrhoea

May give rise to iron deficiency anaemia

45
Q

Colorectal cancer

Left Sided Lesion

A

Present earlier

More likely to cause a change in bowel habit

More likely to obstruct

46
Q

How do you diagnose colorectal cancers?

A

Blood tests
Examination and History
Radiology
Tissue diagnosis

47
Q

Pancreas protein producing capacity

A

13x protein producing capacity of liver

48
Q

Likelihood of colorectal cancer in Transverse colon

A

10%

49
Q

Likelihood of colorectal cancer in Descending colon

A

15%

50
Q

Likelihood of colorectal cancer in Sigmoid colon

A

25%

51
Q

Likelihood of colorectal cancer in Rectum

A

20%