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JMP Semester 2 > Week 17 > Flashcards

Week 17 Flashcards

1
Q

What are the three distinct muscle regions in the oesophagus

A

Superior third- voluntary striated muscle

Middle third- voluntary striated and smooth muscle

Inferior third- smooth muscle

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2
Q

What is Barrett’s oesophagus?

A

Refers to the metaplasia (reversible change from one differentiated cell type to another) of lower oesophageal squamous epithelium to gastric columnar epithelium. Usually caused by chronic acid exposure as a result of a malfunctioning lower oesophageal sphincter. Acid irritates the oesophageal epithelium, leads to potential metaplastic change.

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3
Q

What is the main composition of the oesophagus?

A

External longitudinal muscle

Internal circular layers

Mucosal lining (large obvious smooth layer- changes to ridges at the stomach junction

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4
Q

Where does the oesophagus pass through the diaphragm?

A

Oesophageal hiatus

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5
Q

Where does the oesophagus enter the stomach?

A

Cardial orifice

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6
Q

What are the 4 parts of the stomach?

A

Cardia- closest to the oesophagus

Fundus- upper part of stomach next to the cardia

Body- main part of the stomach

Pylorus- stomach end at the duodenum

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7
Q

How many curvatures does the stomach have and what are they called?

A

Lesser curvature (medial surface)

Greater curvature (lateral surface)

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8
Q

What are the longitudinal gastric folds called and what do they allow for?

A

Rugae- stomach expansion.

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9
Q

What is the pyloric sphincter?

A

It is circular smooth muscle that controls the discharge of stomach contents into the duodenum.

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10
Q

What are the gastric pits?

A

Gastric pits are indentations in the stomach which denote entrances to 3-5 tubular shaped gastric glands. THESE ARE NOT RUGAE.

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11
Q

Where are the gastric glands?

A

They are just next to the gastric pits and empty into these pits.

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12
Q

What are the 4 types of secretory cells in the gastric glands?

A

Chief

Parietal

Mucous

G cells

N.B wont be able to distinguish these without special staining.

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13
Q

What do the 4 secretory cells produce?

A

Chief- pepsinogen and gastric lipase

Parietal- HCl, and intrinsic factor for B12 absorption

Mucous- mucous

G cells- secrete gastrin into the blood (to then act on chief and parietal cells.

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14
Q

How can the pyloric sphincter appear within histology?

A

A large lump of muscle.

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15
Q

How to identify the villi change from the stomach- duodenum?

A

The stomach has villi but in the duodenum it is much longer

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16
Q

What is the name for the mucous gland only found in the duodenum?

A

Brunner’s glands (can be a large lump of gland tissue)

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17
Q

What is the chief function of the small intestine?

A

Absorption of nutrients (90% of this happens in small intestine) Large bowel mainly for water absorption.

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18
Q

What is the general histology of the small intestine wall?

A

Thick mucosa specialised for providing massive surface area

Extensive folding known as “crypts of Lieberkuhn”

Microvilli on apical surface of cells lining the crypts further increase surface area.

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19
Q

What are the absorptive cells that line the crypts and what do they secrete?

A

Goblet cells- secrete mucous

Paneth cells- secrete lysozyme

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20
Q

What main structures secrete into the duodenum?

A

Pancreas

Liver

Gall bladder

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21
Q

Where do these structures secrete into the duodenum?

A

At major duodenal papilla

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22
Q

How are fats absorbed in the small intestine?

A

Through simple diffusion into lacteals. (the lymphatic vessels of the small intestine)

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23
Q

What is the difference between the Jejunum and the Ileum?

A

Jejunum joins the duodenum and the ileum.

Jejunum is in the upper left part of the peritoneal cavity whereas the ileum is lower left.

Ileum is a lot larger that the jejunum.

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24
Q

Where is the circular smooth muscle vs the longitudinal smooth muscle?

A

Circular is inner and longitudinal is outer.

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25
Q

How does the villi compare in the duodenum vs the ileum?

A

Longer in the duodenum.

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26
Q

How can coeliac disease show in histology?

A

A flattening of the villi (from an immune response).

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27
Q

Where is the villi and where is the crypts typically?

A

Villi are long structure protruding out. Crypts are an between villi (kind of burrowing inward.)

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28
Q

What is in a crypt of lieberkuhn?

A

Goblet cells (white circles)

Paneth cells (small red dots (smaller than goblet)

Endocrine cells in the very bottom of the crypt.

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29
Q

What are the clinical signs and symptoms of dehydration? (11)

A

Thirst

Weight loss

Dry mucous membranes

Sunken-appearing eyes

Decreased skin turgor

Increased capillary refill time

Hypotension and postural hypotension

Tachycardia

Weak and thready peripheral pulses

Flat neck veins when the patient is in the supine position

Oliguria- low output of urine between 80 ml-400ml/day. Anuria (<80)

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30
Q

How is hydration be maintained in a patient who has vomiting and/or diarrhoea?

A

Enteral routes preferred (oral rehydration solution) but if that is not possible

NG tube or

IV fluids (with sodium, glucose and potassium chloride)

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31
Q

What fluids should a dehydrated patient get?

A

Some fluids which have glucose, sodium and potassium to ensure best possible absorption of the fluids in the GIT. Of main importance is the sodium glucose symport.

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32
Q

What is Oral rehydration solutions (ORSs)?

A

Specifically designed fluids that contain an appropriate amount of sodium, glucose and other electrolytes and are of the appropriate osmolality, to maximise water absorption from the gut. They use the principle of glucose facilitated sodium transport whereby glucose enhances sodium and secondarily water transport across the mucosa of the upper intestine.

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33
Q

Challenges in maintaining a child/infant with gastroenteritis?

A

Low blood volume increased risk of dehydration

Cannot communicate pain properly

Greater chance of vomit aspiration

Baby would have a lot less exposures like this in general (low immunity)

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34
Q

What are some signs to look out for in a deteriorating infant (infant red flags)

A

Being floppy

Not eating

Stopped interacting

Etc

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35
Q

Infant with gastro/dehydration bad symptoms to look out for?

A

Amount of wet nappies

Increases irritability/crying

Floppy limbs

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36
Q

What are the benefits of the hydrolyte ice blocks?

A

More appealing

Slow introduction of fluid into the system (as ice needs to melt) means less chance of induced vomiting.

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37
Q

What is the clinical features of Staphylococcal food poisoning?

A

Sudden onset of symptoms (1-6 hours).

Lasts 1-2 days

Sudden onset severe Nausea and vomiting. Cramps and diarrhoea may be present

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38
Q

What is the clinical features of Norovirus and rotavirus infection?

A

Onset 12-48 hours after exposure to virus.

Fever, nausea, vomiting (more in children), abdominal cramping, diarrhoea (more in adults), headache.

Lasts 12-60 hours.

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39
Q

What is the clinical feature of salmonella?

A

Onset 6-48 hours

Symptoms- diarrhoea, fever, abdominal cramps, vomiting.

Lasts 4-7days

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40
Q

What is the clinical features of toxin producing organisms like E.coli O147?

A

Onset 1-8 days after exposure.

Symptoms- severve bloody diarrhoea, abdominal pain and vomiting, usually no fever (illness more common in children under 4.

Lasts 5-10 days

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41
Q

What are the symptoms of a clostridium difficile infection?

A

Watery diarrhea 10 to 15 times a day

Abdominal cramping and pain, which may be severe

Tachycardia

Fever Blood or pus in the stool

Nausea

Dehydration

Anorexia (loss of appetite)

Weight loss

Distended abdomen

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42
Q

How should a stool sample be collected?

A

As cleaning as possible trying not to introduce any new bacteria types to the stool.

Not from hands, urine or toilet.

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43
Q

What tests to order on a stool test?

A

MCS- microscopy culture and sensitivity.

OCP- ova, cysts and parasites.

PCR- typing

List more information i.e. suspected gastroenteritis so the pathologist can add anything they also thing is required

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44
Q

What are some challenges of identifying pathogens by culture and microscopy?

A

Growth conditions may be poor

Might be a virus or other particle that is too small to see/wont culture.

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45
Q

What is the common method used for direct antigen detection?

A

Faecal multiplex PCR

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46
Q

How does faecal multiplex PCR work?

A

Primers for an array of common pathogens, can type the pathogen of interest.

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47
Q

How does the amount and outcome of cases of gastroenteritis compare globally?

A

Less cases in Australia, rarely results in death

Lots of cases in developing countries, many deaths result.

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48
Q

Underlying causes of increased mortality from gastroenteritis in some countries?

A

Lack of medical facilities

Poor food prep/storage

No clean drinking water

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49
Q

What is the latent period in disease transmission?

A

The time between an exposure to an infectious organism and the infection of the host by the pathogen. (after infectious host is often infectious to others)

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50
Q

What is the incubation period in disease transmission?

A

The time between exposure and the onset of clinical symptoms (different to latent period)

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51
Q

What is the transmissibility in disease transmission?

A

How it is able to be transferred/spread.

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52
Q

What is the infectious period in disease transmission?

A

The period of time in which the host may spread the pathogen to others.

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53
Q

What is the reproductive rate in disease transmission?

A

The rate in which a single case can generate other cases (how many people one case can infect).

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54
Q

What does Enteral mean?

A

Refers to intake of food via the gastrointestinal (GI) tract.

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55
Q

What can be the effect of taking medications that regulate stomach acidity (reduce)?

A

Can increase risk of bacterial infection as gastric juice not acidic enough to kill them.

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56
Q

What are the red flags for gastroenteritis symptoms?

A

Meningitis

Sepsis

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57
Q

What investigation should be done in the case of Maria?

A

Stool sample- MCS, O&P (ova and protozoan), PCR

Bloods- FBC, CRP, UEC (urine electrolytes count????)

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58
Q

What treatment for Maria?

A

Rehydration IV

Anti emetic (vomit prevention)

Anti-diarrhoeal probably not because of paralytic ileus.

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59
Q

What about a baby with gastro?

A

Might try anti emetics to allow for oral rehydration.

NG tube.

Could do IV but tricky

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60
Q

Should you give someone with diarrhoea gastro antimotility drug?

A

No because it may cause an ileus (paralytic), want to flush out the bug that is causing the issue.

Supportive care of rehydration should be enough.

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61
Q

What is the common lowered electrolytes by diarrhoea?

A

Potassium and bicarbonate

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62
Q

What is a bolus in terms of IV fluid?

A

It is a fast delivery mechanism for IV fluids.

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63
Q

Would you do a stool culture on every gastro case?

A

No because there is way too many, only on bad cases or in an outbreak situation.

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64
Q

Why do small amounts of liquid for rehydration in someone who is vomiting?

A

Large amount can trigger vomiting

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65
Q

Sources of fluid intake and average intake amount?

A

Oral (external)- intake of fluids and food (and/or IV fluids)

Fluid-1500ml, Food-700ml

Metabolic water production (internal) 300mL

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66
Q

What are some ways for fluid loss?

A

Faeces- (200ml)

Sweat- (100ml)

Urine- (1400ml)

Insensible loss- (800ml) (evaporative loss from the respiratory tract and skin (deemed insensible because we are not aware of it.

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67
Q

What is the approximate intake and output of water per day?

A

2500 in and 2500 out.

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68
Q

What are some general volumes for water internal fluxes?

A

Diffusion turnover in the capillaries 80,000L

Lymph flow = 2.5L

Glomerular filtration rate (Kidneys) = 180L

Fluid in the GIT = 8-9L

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69
Q

How much water is lost per day to insensible losses?

A

800mL

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70
Q

How much water is lost by faeces per day?

A

200mL

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71
Q

What are the net fluid movements during ingestion?

A

Food and fluid 1200mL

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72
Q

What are the net fluid movements during secretions?

A

Saliva 1400mL

Gastric juice 2500mL

Bile 600mL

Pancreatic juice 1500mL

Intestinal juice 1000mL

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73
Q

What are the net fluid movements during absorption?

A

7000mL from Small intestine

1000mL from large intestine (can increase up to 5000mL)

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74
Q

What is the net fluid movements during loss?

A

Faeces- 200mL

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75
Q

What is a simple way to summaries the fluid movement in the GIT?

A

Fluid in (ingestion + secretion) - fluid out (intestinal absorption) = fluid lost (faeces)

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76
Q

What is the function of saliva?

A

contains digestive enzymes, mucous, antibacterial compounds and electrolytes Lubricates and softens food, helps to form a bolus. Enzymes begin digestive process (i.e. salivary amylase breaks down starch to glucose)

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77
Q

How is water absorbed?

A

Nutrients and ions are absorbed with transporter proteins

The influx of these nutrients and ions such as glucose, sodium and potassium cause an osmotic gradient.

Water flows down this gradient through the enterocytes and through tight junctions, thus absorbed in the intestines

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78
Q

What is an enterocyte?

A

A cell in the intestinal lining.

79
Q

Where is faeces stored?

A

Stored in the rectum, removed via the anus (defecation).

80
Q

What kinds of control is defecation controlled by?

A

Voluntary and involuntary control.

Rectal distension causes an increase in pressure

This pressure stimulates the intrinsic nerves to increase peristalsis in the sigmoid colon and relax the internal anal sphincter (parasympathetic) (involuntary)

The external anal sphincter is under voluntary control

81
Q

What happens if the external sphincter relaxes?

A

Defecation commences

Puborectalis and levator ani muscles relax

Anorectal angle straightens

Abdominal muscles contract to increase intra-abdominal pressure

Faeces are expelled

82
Q

What is the Vasalva manoeuvre?

A

The Valsalva maneuver is performed by moderately forceful attempted exhalation against a closed airway, usually done by closing one’s mouth, pinching one’s nose shut while pressing out as if blowing up a balloon.

Can assist defecation

83
Q

What happens if the external sphincter does NOT relax?

A

Urge to defecate is overridden

Rectum dilates to accommodate increased volume

84
Q

What is faecal continence? .

A

The control of defecation, a learned behavior in early childhood.

Maintained by health of the rectum and anal canal and proper nerve/muscle function involved in defecation

85
Q

What is the anal sampling reflex?

A

A reflex allowing for the upper anal canal to determine between flatus and faeces. And selectively relax for flatus to reduce pressure.

86
Q

What is faecal incontinence?

A

Improper control of defecation

Symptom not a diagnosis

87
Q

What is the most common causes of faecal incontinence?

A

Structural anorectal abnormalities - Sphincter trauma, perianal fistula, rectal prolapse, weakness of the pelvic floor (traumatic childbirth/surgery)

Neurological disorders - MS, spinal cord injury, stroke

Altered bowel habits - Diarrhoea, inflammatory bowel disease, chronic constipation (overflow incontinence), drugs (orlistat)

88
Q

Define diarrhoea.

A

Defined as having more than three loose or liquid bowel movements/day or producing more stool than is considered normal for a particular patient

Can be acute/self limiting (usually infective cause) or chronic (underlying disease)

89
Q

What are the three main types of diarrhoea?

A

Secretory

Osmotic

Exudative/inflammatory

90
Q

What is secretory diarrhoea

A

Occurs due to alterations in water absorption, particularly secretion of fluid into the intestinal lumen (more than the absorption)

91
Q

What is the common causes for secretory diarrhoea?

A

Bacterial endotoxins eg cholera toxin

causes prolonged openings of cellular chloride channels, chloride going into the lumen drive osmotic movement of water into the lumen as well.

Cholera toxin also interferes with enteric nerves to cause increased fluid secretion.

Certain laxatives (increase intestinal secretion)

Drugs/toxins- (increased secretion)

Neuroendocrine Tumors- particularly carcinoma of the pancreatic islets can cause increased intestinal secretions via Vasoactive intestinal peptide (VIP)

92
Q

What is Osmotic diarrhoea?

A

Diarrhoea caused by excessive solutes in the intestinal lumen (driving osmosis of water into lumen)

93
Q

What is the two main causes for osmotic diarrhoea?

A

Ingestion of a non-absorbable molecule

Malabsorption

Damaged intestinal lining (eg Coeliac)

Non-absorbed nutrients in the large intestines

intolerance

94
Q

What is the cause Exudatives/Inflammatory diarrhoea?

A

Tissue damage reduces absorptive capacity and compromises the integrity of the mucosal barrier- fluids leak into the lumen.

95
Q

Common causes of Exudative/Inflammatory diarrhoea?

A

Infections

viral (ebola)

bacterial (e.coli, salmonella)

parasitic (Entamoeba histolytica)

Inflammatory bowel disease

Ulcerative colitis

Crohn’s disease

96
Q

What is blood associated with diarrhoea termed?

A

Dysentery ( usually associated with serious infection)

97
Q

What is blood on toilet paper termed?

A

Haematopapyrus- associated with anal fissures, haemmorhoids

98
Q

What is melena?

A

Passage of tarry, darker blood, associated with upper GIT bleeding (peptic ulcers)

99
Q

What is nausea?

A

Feelings of unease and discomfort in the upper stomach.

100
Q

What is Retching?

A

Spasmodic respiratory movements against a closed glottis

Antrum (base) of stomach contracts, rest of stomach relaxes

101
Q

What is Vomiting? (emesis)

A

Hypersalivation occurs to lubricate mouth.

Deep breath taken (to avoid aspiration)

Glottis closed

Larynx raised to open the upper oesophageal sphincter

Soft palate raised to close the nasal cavity

Retro-peristalsis starts to move contents from duodenum into stomach

Diaphragm contracts downwards, negative pressure created in thorax, oesophagus and lower oesophageal sphincter opens.

Abdominal muscles contracted, stomach is squeezed with pyloric sphincter closed and oesophagus open (drives up)

102
Q

How is vomiting controlled?

A

Neural pathway - vomitation centre

Humoral Pathway- “Chemoreceptor trigger zone”

103
Q

Where are the vomiting pathways controlled?

A

Two brain centres

vomitation centre and the chemoreceptor trigger zone

104
Q

What is the neural pathway for vomiting?

A

The vomitation centre (within the reticular formation of the medulla) when activated triggers vomiting.

The vomitation centre receives information from:

Chemoreceptor trigger zone

Visceral afferents from the GIT (signal GIT distension, irritation)

Visceral afferents from outside the GIT (bile duct or heart)

Afferents from the other centres of the brain (odours, fear, vestibular disturbance-motion sickness)

105
Q

What is the Chemoreceptor trigger zone- Humeral pathway?

A

It is located within the brainstem (just under the fourth ventricle)

Outside the blood brain barrier

Chemoreceptors detect multiple chemical emetic stimuli including emetic drugs(ipecac), uremia, hypoxia and ketoacidosis.

106
Q

What are some important electrolytes in body function?

A
  1. Sodium- water balance, nerve and muscle function
  2. Potassium- water balance, nerve and muscle function
  3. Calcium- nerves, muscles, bones, blood movement, hormones etc
  4. Bicarbonate- regulate pH/acid balance in the body
  5. Magnesium- nerve, muscle, immune, blood glucose, energy, protein synthesis
  6. Chloride- fluid regulation
  7. Phosphate- bones, teeth, energy, membranes, DNA
107
Q

What is osmolality?

A

Amount of solutes per kg of solvent.

Not affected by temp or pressure

108
Q

What is osmolarity?

A

Amount of solute per L of solvent.

Affected by temp and pressure

109
Q

Define Isotonic

A

Solutions with same osmotic pressure (no water movement (RBC will stay the same))

110
Q

Define Hypotonic

A

Lower osmotic pressure, more solutes inside the cell, water movement into RBC (swelling)

111
Q

Define Hypertonic

A

Higher osmotic pressure, water movement outside the RBC (shriveling)

112
Q

What are the location in and out of cells for common electrolytes?

A
  1. Outside the cells- sodium and chloride

2. Inside the cells- Potassium, magnesium, phosphate and sulfate.

113
Q

What is the importance of Sodium and thus sodium homeostasis?

A
  1. Most abundant cation in ECF, main determinant of plasma osmolality
    1. Regulates- heart, nerve and muscle functions.
114
Q

What is the terms for sodium loss or increase in the blood?

A
  1. Hyponatraemia (low blood sodium)

2. Hypernatraemia (high blood sodium)

115
Q

What is some common causes for Hyponatraemia?

A
  1. Excess fluid in the body relative to sodium- drinking too much or kidney problem
    1. Excessive loss of Sodium- chronic severe diarrhoea/vomiting (rarely from decreased sodium intake)
    2. In general hyponatraemia drives water from the Extracellular fluid into cells (ICF)
116
Q

What are some common symptoms for Hyponatraemia?

A
  1. Headache
    1. Nausea
    2. Vomiting
    3. Cramps
    4. Seizures
    5. Confusion
    6. Coma
117
Q

What is some common causes for Hypernatraemia?

A
  1. Excessive water excretion/loss
    1. Diminished thirst sensation/water deprivation (diuretics, diabetes, CNS disorder
    2. In general leads to a shift of water from the ICF (In cells) to ECF (outside cells)
118
Q

What are some symptoms for Hypernatraemia?

A
  1. Thirst

2. Confusion

119
Q

What is the importance of potassium and thus potassium homeostasis?

A
  1. Potassium is a major intracellular cation
    1. Crucial to neuromuscular and cardiac function
    2. Serum potassium levels maintained by absorption and excretion regulated by the hormone aldosterone.
120
Q

What is the terms for high or low potassium in the blood?

A
  1. High- Hyperkalaemia

2. Low- Hypokalaemia

121
Q

What is a common cause of Hyperkalaemia?

A

Renal disease

122
Q

What is some symptoms of Hyperkalaemia?

A
  1. Abdominal cramping
    1. Fatigue
    2. Muscle weakness/paralysis
    3. Slower cardiac conduction (in severe cases)
123
Q

What is another potential affect of disturbed K+ homeostasis?

A
  1. Affected intracellular pH

2. Acid-base disturbance can cause this K+ imbalance

124
Q

What is the effect of Acidosis on K+?

A

Causes a shift of K+ from the ICF to the ECF (in exchange for H+).
This drives Hyperkalaemia.

125
Q

What is the effect of alkalosis on K+?

A

Cause a shift of K+ into the cell.

Driving Hypokalaemia.

126
Q

How do water molecules move through the small and large intestine?

A
  1. Paracellular routes - pass between cells through “loose” tight junctions. This types reduces down the length of the small intestine and further towards the colon
    1. Transcellular routes- pass directly through cell membranes through water channels (aquaporins) (requires both active and passive transporters.
127
Q

What is the key driver of water movement across intestinal epithelium?

A

Osmotic pressure - driven by the selective distribution of Na+, K+ and Cl- across compartments.

128
Q

Where are most ions absorbed?

A

The small intestine actively absorbs the most ions.

129
Q

How is the driving force for osmotic pressure generated?

A

Basolateral Na+/K+-ATPase generates force for most absorption and secretion across the membrane.

130
Q

How are the various electrolytes absorbed in the small intestine?

A
  1. Sodium- actively absorbed (enhanced by sugars and neutral amino acids) (both the jejunum and the ileum)
    1. Potassium- passively absorbed when concentration rises from water absorption. (both the jejunum and the ileum)
    2. Chloride- absorbed (jejunum), absorbed in exchange for HCO3- (Ileum)
    3. HCO3 (bicarbonate)- Absorbed (jejunum) secreted partly in exchange for Cl- (ileum)
131
Q

How are various electrolytes absorbed in the large intestine (colon)?

A
  1. Sodium- actively absorbed
    1. Potassium- net secretion when K+ concentration is low in the lumen.
    2. Chloride- absorbed in exchange for HCO3-
    3. HCO3 (bicarbonate)- secreted partly in exchange for Cl-
132
Q

What is the effect of diarrhoea on electrolytes

A
  1. In acute diarrhoea these is a failure to reabsorb fluids secreted into intestine or intestine overproduces fluid + changes in permeability of mucosa.
    1. This means a loss of electrolytes and water.
    2. The lost H2O and electrolytes are replaced from blood which can lead to dehydration and electrolyte imbalance.
133
Q

What is the effect of diarrhoea on acid-base balance?

A
  1. Electrolytes that are lost from the blood include HCO3- loss as HCO3- is produced in intestinal lumen after massive loss of bicarbonate.
    1. This drop in HCO3- in blood leads to acidosis
134
Q

What are the three ways vomiting causes fluid loss?

A
  1. By ejecting fluids already taken by mouth
    1. Limiting further intake of normal fluid volumes
    2. By ejection of fluids secreted into the upper intestine, primarily gastric juices.
135
Q

What is the effect of vomiting on electrolytes?

A
  1. In the blood:
    • HCO3- gain
    • Loss of Cl-
  2. In the gastric lumen:
    • Secretion of HCl (pH decreases)
    • Secretion of K+
136
Q

What can vomiting show in a blood analysis?

A
  1. Metabolic alkalosis (from increase in HCO3-)
  2. Hypochloraemia (from loss of Cl-)
  3. Hypokalaemia (through direct loss of K+ and exchange of K+ for Na+ in the kidneys when dehydrated)
137
Q

What does the autonomic nervous system do?

A

Automatic responses

138
Q

What does the sympathetic nervous system do?

A

Fight or flight

139
Q

What does parasympathetic nervous system do?

A

Rest and digest

140
Q

Where does most of the parasympathetic control fibres originate?

A

The overwhelming amount of parasympathetic fibres emerge from the brainstem. Do not require the spine. The other origins are from the lumbar vertebrae for the bladder and genitals.

141
Q

Where does the sympathetic control fibres originate?

A

From various levels in the spinal cord. If you are paralyzed would impact on the sympathetic more.

142
Q

What is the neurotransmitters used by the parasympathetic fibres?

A

Always ACh onto receiving tissue. Needs to be heavily controlled in GIT otherwise tissue would all contract at the same time from Ach.

143
Q

What is the neurotransmitters used by the Sympathetic fibres?

A

Noradrenaline for most of its synapses except for skin, blood vessels of the skin, sweat glands there is ACh released.

144
Q

What is the significance of parts of the sympathetic fibres using ACh and using acetylcholinesterase inhibitors or muscarinic agonists?

A

There will be side effects affecting the sympathetic fibres as well as increased GIT activity such as sweating and flushed skin.

145
Q

What are the main muscarinic receptors of the GIT?

A

M3 is main, but there is also M2.

146
Q

What is the general effect of released ACh on the M3 receptors in the GIT?

A
  1. ACh release
    1. M3 receptors activate
    2. Increase the enteric plexus activity
    3. Contraction of the smooth muscle
    4. Increase in GIT motility and secretions
    5. Aids digestion
    6. Promotes defecation.
147
Q

What is the effect of too much GIT motility?

A

Diarrhoea.

148
Q

What is the exact mechanism of the muscarinic receptors?

A
  1. Muscarinic receptors coupled to Phospholipase C
    1. Activation of Phospholipase C causes an increase in IP3
    2. There are IP3 receptors on the Sarcoplasmic reticulum calcium store
    3. Liberate Ca++
    4. Increased muscle contraction.
149
Q

What are the sympathetic molecules that have impact on the GIT?

A

Adrenaline (hormone) and noradrenaline (neurotransmitter).

150
Q

What are the sympathetic molecules receptors in the GIT?

A

Alpha 1, alpha 2 and Beta 2 adrenergic receptors.

151
Q

What is the general action of the sympathetic molecules in the GIT?

A
  1. Adrenaline and noradrenaline bind to alpha 1 and 2 , Beta 2 adrenergic receptors.
    1. These receptors cause inhibiting of the enteric plexus activity
    2. Relaxation of the smooth muscle
    3. Decrease in GIT motility.
152
Q

What happens with a decrease in GIT motility?

A

Constipation.

153
Q

What is diarrhoea a disorder of?

A

Disorders affecting intestinal water or electrolyte transport.

- Failure to reabsorb fluids secreted in the intestine, produce too much fluid and change K+ permeability of the mucosa
- More liquid stool than normal.
154
Q

What are the treatment approaches for Diarrhoea?

A
  1. Maintenance of fluid and electrolyte balance
    1. Use of anti-infective agents (antibiotics)
    2. Use of spasmolytic (reduces smooth muscle spasm) or other antidiarrhoeal agents (opioids)
155
Q

What are the main opioid receptors in the GIT?

A
  1. u- opioid receptors

2. δ1 - (delta) opioid receptors

156
Q

What is the effect of the u and δ1 receptors?

A

U- decreases GIT motility
δ- decreases GIT secretions
If both are stimulated there will be effects on absorption.

157
Q

What is loperamide?

A

It is a opioid receptor agonist (u receptor)

158
Q

What is loperamides (opioid receptor agonist) mechanism of action?

A
  1. U- receptor activation
    1. Inhibits ACh release
    2. Relaxes longitudinal and circular muscle of the intestine
    3. Reduces GIT motility
    4. (may also reduce GIT secretions)
    5. Can cause a side effect of constipation.
159
Q

Can the opioid receptor agonist loperamide have an effect on the CNS?

A
  1. No. because it has been designed to not pass through the blood brain barrier.
    1. It is actually 40-50 times as potent as morphine
    2. Because it will not have CNS effect can be sold over the counter
160
Q

What is functional diarrhoea?

A

It is a chronic form of diarrhoea that is due to excessive amounts of bile salts in the GIT - leading to excessive water and electrolyte excretion –> diarrhoea.

161
Q

What is the treatment for function diarrhoea?

A

Cholestyramine

162
Q

What is the mechanism of action for cholestyramine?

A
  1. Binds to bile salts, lipid soluble vitamins (A,D,E,K), other drugs and some bacterial toxins.
    1. Grabs onto dietary cholesterol
163
Q

What is the issues with cholestyramine?

A
  1. Non selective binding
    1. Chemical antagonist
    2. Will interfere with absorption of lipid soluble vitamins as well as other drugs (so will interfere with other drugs.
    3. May cause constipation
164
Q

What are the neurotransmitters and neuropeptides that trigger nausea and vomiting?

A
  1. Serotonin- 5-HT3 receptor
    1. Dopamine- dopamine D2 receptor
    2. Acetylcholine- muscarinic M1 receptor
    3. Histamine- Histamine H1 receptor
    4. Cannabinoids CB1 receptor
      Substance P- action on the neurokinin NK1 receptor
165
Q

What is the mechanism of action for serotonin receptor antagonists (odansetron) in reducing vomiting?

A
  1. Serotonin released by enterochromaffin cells in small intestines in response to chemotherapy
    1. Ondansetron (“Setrons”) inhibit 5-HT3 receptors on vagal afferents in periphery.
    2. This prevents signal to the CNS
    3. Also Inhibits signal centrally at the CTZ (chemoreceptor trigger zone) and STN (solitary tract nucleus)
    4. Prevents activation of emetic centre
    5. Stops vomiting.
166
Q

What is the mechanism of action for dopamine receptor antagonists in reducing vomiting?

A
  1. Metaclopramide, domperidone
    1. Inhibit dopamine D2 receptors at the CTZ (chemoreceptor trigger zone) and STN (solitary tract nucleus).
    2. Increases coordination of GIT motility from complex action of dopamine receptor inhibition causing RESTORED balance of ACh release onto GIT smooth muscle.
    3. As a bonus is also has weak antagonist action at 5-HT3 receptors (serotonin) and some can block histamine and muscarinic receptors.
167
Q

What is the mechanism of action for neurokinin receptor antagonists in reducing vomiting?

A
  1. Eg, aprepitant.
    1. Neuropeptide substance P causes vomiting and is released by vagal afferents.
    2. Neurokinin NK1 receptor antagonists block the effect of substance P in the CTZ and STN.
168
Q

What is the mechanism of action for antihistamine in reducing vomiting?

A
  1. Can be antihistamine promethacine, cyclizine (also blocks M1 receptors).
    1. Most effective for motion sickness and vestibular disturbance
    2. Blocks effects of histamine in vestibular afferents and histamine H1 receptors in the STN (solitary tract nucleus).
169
Q

What is the mechanism of action for muscarinic receptor antagonists in reducing vomiting?

A
  1. Can be hyoscine, hydrobromide
    1. Most effective for motion sickness and vestibular disturbances
    2. Blocks effects of Acetylcholine in vestibular afferents.
170
Q

What anti-emetic drug types would be used for cytotoxic drug induced emesis?

A
  1. 5-HT3 receptor antagonists- (reduce serotonin effect) ondansetron.
    1. Centrally acting dopamine receptor antagonists.
    2. Neurokinin NK1 receptor antagonists- aprepitant.
171
Q

What anti-emetic drug types would be used for vestibular/motion sickness?

A
  1. Antihistamines (H1 receptor antagonists) cyclizine, promethazine.
    1. Muscarinic M1 receptor antagonists- hyoscine, hydrobromide
172
Q

What is commensal microorganisms?

A

Living on or in another organism and deriving benefit without causing harm or benefit to the host.

173
Q

What is a microbial Niche?

A

All microbial species are thought to occupy a unique niche (a way they utilise their environment to thrive)
More specifically in humans niche is determined by their specific metabolic properties and requirements of the specific microbe (aerobic/anaerobic, pH, immune system etc)

174
Q

How does type and amount of bacteria change along the GIT?

A
  1. Towards the top more aerobic bacteria as more O2.

2. Less microbes in stomach as acidic, slightly more in SI and lots in LI

175
Q

What is immune homeostasis?

A

The re-seeding of the gut microbiota after the bacterial community structure is altered or certain species are depleted from the lumen.

176
Q

What specific niches may be crucial to facilitate immune homeostasis?

A
  1. Crypts
    1. Inner mucus layer
    2. Appendix
177
Q

What stages can immune homeostasis be broken down into?

A
  1. Steady state- some microbes are able to penetrate the inner mucus layer and enter crypt spaces.
    1. Environmental challenges
      - Diet change
      - Antibiotic consumption
      - Abnormalities in GIT motility
    2. Recovery- the crypts and mucosa serve as reservoirs to repopulate the lumen after environmental challenges
178
Q

What are some factors that affect the composition of microbial communities?

A
  1. Diet
    1. Other environmental factors
    2. Host factors (immune system)
179
Q

What is symbiosis?

A

Interaction between two organisms in close physical association which benefits them both.

180
Q

What is Dysbiosis and what can cause it?

A

Is an unhealthy change in the normal bacterial ecology in a part of the body via:
1. Loss of beneficial microbes
2. Expansion of pathological microbes
Loss of diversity

181
Q

What is the difference between the Systemic Immune system and the Mucosal Immune system?

A
  • Systemic immune system is largely a sterile environment- vigorous response to microbial invasion
    Mucosal Immune system (oral, rectal, vaginal, nasal) has a constant exposure to foreign matter (less responsive to foreign antigens)
182
Q

What is the role of the public health unit?

A

Identify and prevent or minimise public health risks in the community.

183
Q

What is an Outbreak?

A

A disease outbreak is the occurrence of cases of disease in excess of what would normally be expected in a defined community, geographical area or season. An outbreak may occur in a restricted geographical area, or may extend over several countries.

184
Q

What is an Epidemic?

A

A widespread occurrence of an infectious disease in a community at a particular time.

185
Q

What is a Pandemic?

A

A disease prevalent over a whole country or the world.

186
Q

What is a Sporadic disease?

A

Occurring occasionally, singly, or in irregular or random instances

187
Q

How are outbreaks of disease recognised?

A
  1. Pathogen surveillance
    1. Notification by astute clinicians (epidemiological links)
      Reports by the public (direct or via NSWFA)
188
Q

What makes an investigation of an outbreak worthwhile?

A
  1. Prevent from happening again. (adjust policy/practice)
    1. Find the source to stop its continued impact.
    2. Training new staff
      Reassuring the public
189
Q

What are the steps in an outbreak investigation? (10 steps)

A
  1. Verify the diagnosis and confirm outbreak.
    1. Prepare to investigate
    2. Case definition
    3. Initiate case findings
    4. Perform descriptive epidemiology
    5. Generate hypothesis
    6. Test hypothesis
    7. Environmental investigation
    8. Implement control/prevention measures
    9. Communicate findings
190
Q

What is the different types of case definition?

A

Case definition can be for disease or a particular outbreak
1. Disease- definition wont change
Outbreak- may change during the outbreak but will only be used for that particular outbreak. Sensitive –> specific

191
Q

Main types of studies are?

A

Experimental and observational

192
Q

What are the main types of studies used for outbreak investigation?

A

Observational studies:

  1. Cohort study
  2. Case control study
193
Q

When is a cohort study typically used for outbreak investigation?

A
  1. Well defined population
    1. Can identify a population at risk
      Risk is expressed as relative risk

JMP Semester 2 (8 decks)

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