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Week 18: Abdominal Pain > abdominal pain > Flashcards

abdominal pain Flashcards

1
Q

what are the 3 phases of gastro-intestinal tract function?

A
  1. cephalic - gastric secretions that occurs before food enters stomach
  2. gastric - digestive secretions after you swallow food, stimulated by increase in stretch and pH of stomach
  3. intestinal - duodenal response to arriving chyme
  • co-ordinated function of the GIT by integration of neural and hormonal signals
  • temporal overlap between phases and feed-back/forward pathways
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2
Q

what are the 3 types of cells in a salivary gland and what is their role in salivation

A
  1. Acini cells:
    - secrete primary isotonic secretion
    - NA+, Cl-, K+, HCO3-
    - amylase ad mucin production
  2. myoepithelial cells:
    - stimulate ejection of primary secretion into duct
  3. duct cells:
    - secondary modification into hypotonic solution
    - reabsorb Na+, Cl-
    - add K+
    - HCO3- altered depending on flow rate (high = increases, low = decreased)
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3
Q

what are the primary regulatory events in the cephalic phase?

A

BRAIN HIGHER INTEGRATING CENTRES: smell, think, see food

parasympathetic branch:

  • increases saliva secretion
  • increases HCl, mucus, pepsin, gastrin secretion in the stomach
  • stimulates bile ducts, hepatocytes and pancreatic acinar cells

sympathetic branch:

  • increases blood flow to glands and saliva production
  • increase blood flow to stomach
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4
Q

what are the primary regulatory events in the gastric phase?

A

FOOD ENTERS STOMACH

inputs:

  • parasympathetic pathways
  • decreased acidity in stomach due to buffering of food
  • distention of antrum
  • protein, peptides and amino acids

cause:
G cells -> gastrin

effect:

  • increase gastric motility
  • increase parietal cells secretion of HCl
  • trophic maintenance of GI epithelium
  • negative feedback: HCl to G cells
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5
Q

what are the primary regulatory events in the intestinal phase?

A

PRESENCE OF FOOD IN DUODENUM

  • duodenal peptides/ amino acids cause release (pH>3) or inhibit (pH<2) gastrin
  • duodenal fats and breakdown products cause release of secretin and Cholecystokinin
  • acid entering intestines causes secretin release
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6
Q

what factors increase or decrease secretion of saliva?

A

increase:

  • parasympathetic (dominant in normal situations - large vol of watery, enzyme rich saliva)
  • sympathetic (dominant in stressful situation - small vol of thick mucousy saliva)

decrease:

  • sleep
  • dehydration
  • atropine
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7
Q

what factors increase or decrease gastric secretion (HCl, pepsinogen, mucous and intrinsic factor)?

A

increase :

  • gastrin
  • acetylcholine
  • histamine
  • parasympathetic

decrease:

  • H+ in stomach
  • chyme in duodenum
  • somatostatin
  • atropine
  • cimetidine
  • omeprzole
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8
Q

what factors increase and decrease the secretion pancreatic secretions (HCO3-, lipase, amylase and proteases)

A

increase:

  • secretin
  • cholecystokinin (potentiates secretin)
  • parasympathetic supply

decrease:
-sympathetic supply

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9
Q

what factors stimulate biliary secretion (bile salts, pigments, cholesterol, phospholipids, HCO3-)?

A
  • secretin (bile production),
  • cholecystokinin (gallbladder contraction; relaxation of sphincter of Oddi)
  • some central and enteric nerve input
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10
Q

what factors increase and decrease secretions in the large intestines (alkaline mucus (no digestive enzymes))?

A

increase:

  • acetylcholine
  • vasoactive intestinal peptide

decrease:

  • adrenaline
  • somatostatin
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11
Q

describe the 2 phases of swallowing

A
  1. oropharyngeal (1sec)
    - oral phase: holding of formed bolus by tongue against hard palate
    - oral transit phase: lifting bolus onto front of tongue then pushing it towards pharynx (all or nothing reflex as it enters pharynx)
    - pharyngeal phase: elevation and retraction of velum (soft palate) + velopharyngeal closure. movement of base of tongue and pharyngeal muscles push bolus further, larynx closes and upper oesophageal sphincter opens
  2. oesophageal (4-10secs):
    - brain (swallowing centre in medulla) triggers primary peristaltic wave
    - circular muscles behind and longitudinal in front of bolus
    - secondary wave if food is sticky or lodged (more forceful)
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12
Q

name the different cells types of an oxyntic (gastric) gland found in the fundus/body of stomach and their secretions. what other cells are found in the stomach?

A

Chief cells secrete pepsinogen
parietal cells secrete HCl and intrinsic factor
mucous neck cell secrete mucous

G cells in antrum secrete gastrin (to circulation)
mucus cells in antrum secrete mucous

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13
Q

HCl secretion is inhibited when it is no longer required i.e. when the food enters duodenum. What other way is it inhibited?

A

via somatostatin

direct pathway: binds to parietal cells
indirect pathway: inhibit histamine and gastrin release (gastrin triggers HCl release)

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14
Q

what stimulates pepsinogen secretion and what activates it?

A
  • response to vagal stimulation
  • triggered by local H+

HCl activates pepsinogen to pepsin

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15
Q

what is the most serious consequence of loss of secretory function of the stomach?

A

pernicious anaemia

intrinsic factors required for vitamin B12 absorption by receptor mediated endocytosis

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16
Q

what are the cells involved in pancreatic secretion?

A

centroacinal cells:
-secrete aqueous component

acinar cells:
-secrete enzymes: pancreatic amylases and lipases in active form. pancreatic proteases in inactive form (activated in duodenum)

duct cells:

  • secrete aqueous component
  • modification of ion component (rich in HCO3-)
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17
Q

what are the 3 major pancreatic proteolytic enzymes initially stored in zymogens to prevent self digestion?

A
  1. trypsinogen- activated by enterokinase in enterocytes and trypsin itself via +ve feedback -> trypsin
  2. chymotrysinogen - activated by trypsin -> chymotrypsin
  3. procaroxypeptidase - activated by trypsin -> carboxypeptidase
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18
Q

what triggers pancreatic acinar cells to produce enzymes and ductal cells to produce ions (e.g. HCO3-)

A

acinar cell trigger = cholecystokinin secreted by I cells of duodenum in response to amino acids, small peptides and fatty acids (potentiated by vagal Ach)

ductal cell trigger = secretin from S cells of duodenum in response to chyme reaching duodenum (potentiated by vagal Ach and CCK)

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19
Q

relate CCK and secretin production to bile secretion and effect

A

CCK triggers release of stored bile, gall bladder contraction and sphincter of Oddi relaxation. leads to digestion

secretin triggers HCO3- rich bile secretion. leads to neutralisation of H+ in duodenum and micelle formation

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20
Q

define retropulsion, segmentation and haustration of the GIT

A

retropulsion =Stomach contractions originating at antrum and going backward, to prevent too rapid of gastric emptying

segmentation = Mixing and churning of materials without propelling them forward in the tract. predominately in small intestine

haustration = Slow segmental movements that move food very slowly through colon. This movement is going on continually

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21
Q

A person may feel uncomfortable when they are too full, or they are very hungry. Explain why this may be

A
  • Too Full – the receptive relaxation quality of the stomach means that we can store a lot of food without altering pressure -> signals to the feeding and satiety centers in the hypothalamus and appetite center in the amygdala take time to register as it doesn’t just depend on stretch receptors but a lot of other signals combined -> you can continue to eat without realizing that you have reached your limit
  • Too Hungry? Peristaltic waves from the fundus to the body to the antrum of the stomach cause this uncomfortable feeling when the stomach is empty
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22
Q

what conditions cause changes in capillary pressures resulting in oedema?

A
  • cardiac failure: raise in venous pressure -> less osmotic pressure pulling fluid back into the capillaries
  • liver failure: less albumin concentrating in the circulation -> smaller osmotic pressure
  • leaky capillaries in anaphylaxis or sepsis
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23
Q

define insensible fluid loss

A

Water loss that can’t be measured e.g. trans epidermal diffusion and evaporative loss from respiratory tract

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24
Q

give examples of disease processes that will increase fluid losses

A
  • anything that increases respiratory rate e.g. COPD, sepsis, CF, asthma
  • burns
  • infections e.g. pyrexia
  • diarrhoea (e.g cholera)/ vomiting
  • diabetes: polyuria
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25
Q

what 5 steps should you think about before prescribing fluids?

A

1) What is the condition they are suffering from?
2) Does it cause fluid loss?
3) Does the treatment they are receiving cause water loss e.g. diuretics?
4) Are they under filled, over filled, or normal fluid levels? (your review history and symptoms and signs – think of hypovolemic and over loaded symptoms)
5) Do I have to give them IV fluid or can I give oral fluid? (oral fluid is safer)

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26
Q

list hypovolemic and hypervolemia signs (e.g. think vital signs)

A

hypovolemic:

  • postural BP!
  • hypotension (<100mmGh)
  • tachycardia (>90bpm)
  • capillary refil >2secs
  • tachypnoeic (20breaths/min)
  • low urine output (<0.5mls/kg/hr)
  • dry mucous membranes
  • response to passive leg raise

hypervolemic:

  • oedema
  • dyspnoea
  • orthopnoea
  • raised JVP
  • inspiratory crackles at lung bases
  • Hx of cardiac or renal problems
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27
Q

What investigations may be useful to determine volume status?

*think is my pt’s kidneys or heart failing?

A
  • FBC (check Hb if lost blood volume)
  • U&E’s (if kidney failing would see rise in urea and creatinine and fall in eGFR)
  • CXR (sign of heart failure)
  • lactate (raised in hypovolemic shock)
  • urine biochemistry (concentrated urine if kidneys failing)
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28
Q

what’s the difference between a colloid and crystalloid fluid?

A

colloid contains big protein particles that enter the IV space and stay there. resuscitation fluid that can be administered quickly (administration of 500ml but reassess after 15mins (can repeat up to 2L)). high risk of anaphylaxis

crystalloids can pass freely through semi-permeable membrane and are usually for maintenance

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29
Q

what cautions must you take when prescribing fluids?

A
  • Weight of patient
  • Elderly or frail
  • Renal impairment
  • Cardiac failure
  • Malnourished or at risk of refeeding syndrome
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30
Q

what is the limit of time you can prescribe fluids for?

A

24hours

31
Q

what would CXR show on patient who is over filled?

A
  • Alveolar shadowing – fluid filled
  • Kerley B lines
  • Cardiomegaly
  • Upper lobe Diversion – vessels get ‘juicer’
  • Effusion – blunting of costophrenic angles
32
Q

what are the 3 types of fluid you can give and give an example

A

maintenance: 0.18% saline and 4% dextrose
replacement: 0.9% NaCl and balanced salt solution.THIS FLUID IS IN ADDITION TO MAINTENANCE

resuscitation fluid: 4.5% albumin supplied in 0.9% NaCl

33
Q

why is it important to elicit a sexual Hx in a female pt presenting with abdominal pain?

A

exclude ectopic pregnancy

34
Q

list some of the red flags of abdominal pain

A 
sudden onset
haematemesis
unexplained weight loss
change in bowel habits >3weeks
unexplained PV bleeding
shortness of breath
dysphagia
new onset dyspepsia
testicular pain
fever

*symptoms that may indicate MI, perforated viscus, ruptured AAA, ectopic pregnancy, acute pancreatitis, diverticulitis, appendicitis etc

35
Q

what blood tests are useful in someone presenting with abdo pain

A

FBC - raised WBC may indicate infection
CRP - infection or inflammation
Amylase - acute pancreatitis
LFT - abdo pain because of disease of liver or gallbladder

36
Q

what surgical sieve can you use to help with differential diagnosis?

A 
VITAMIN
vascular
infective/inflammatory
traumatic
autoimmune
metabolic
iatrogenic/idiopathic
neoplastic

in abdominal pain think inflammation, perforation, obstruction, vascular, urological, trauma, cardio-respiratory disease

37
Q

compare IBD and IBS

A

IBD:

  • chronic inflammatory condition
  • associated with iliac fossa pain
  • surgical intervention may be required
  • can affect all areas of the GIT (mainly CD)
  • diagnosis confirmed by endo/colonoscopy
  • associated with bloody diarrhoea
  • caused by abdominal response to the immune system

IBS:

  • functional disorder
  • generalised abdominal pain
  • surgical intervention is not necessary
  • only distributed in area of intestines
  • diagnosis made on pt Hx, no organic cause
  • associated with changes in bowel habits often exacerbated by stress
  • caused by disturbance to how the gut and brain interact
38
Q

ulcerative colitis and crohns disease have similar clinical presentations. what are the presentations and how would you differentiate between the 2 chronic IBD?

A
  • abdominal pain typically RIF for CD and LIF for UC or umbilical pn)
  • bloody diarrhoea (+/- mucous)
  • fever
  • tenesmus
  • incontinence
  • weight loss
  • fatigue
  • 14-40yrs onset

differentiate:

  • histopathology from tissue biopsies:
  • endo/colonoscopy
  • negative stool culture

**CD can affect the entire GIT and is segmental and patchy (skip lesions), often with rectal sparing. there is transmural inflammation and perhaps the presence of fissures, sinuses, fistulas and epithelioid granulomas.

**UC inflammation only affects the colonic mucosa and is diffuse and continuous, starting at the rectum and spreading proximally. the disease pattern is more sever distally and doesn’t form fissures, sinuses or fistulas

39
Q

what is the presentation and pathophysiology of diverticular disease? why might it cause abdominal pain?

A
  • common in older generation
  • altered bowel habits +/- LIF colic relieved by defecation
  • nausea
  • flatulence
  • intermitted blood in stool
  • no muscular layer around diverticular - mucosa and submucosa herniate through the muscular layer of the colonic wall
  • pain because it is associated with chronic constipation. herniation may be compacted with faeces which can lead to ischemia/ perforation/ infection of peritoneum. infection/inflammation f the diverticulum is called diverticulitis and is usually what causes symptoms. diverticular disease can be asymptomatic
40
Q

what should you consider in a patient who present with blood in stool and is over 55years

A

colon cancer until proven otherwise

benign cause = polyps

41
Q

list general biopsychosocial factors that may present with abdominal pain

A

•Biological

  • tissue damage/ disease
  • pain intensity and pain quality
  • physical functional interference
  • sleep disturbance

•Social

  • interpersonal relationships
  • work/disability
  • cultural influences
  • environmental factors

•psychological

  • emotional distress
  • attention
  • attitudes and beliefs
  • coping skills
  • pain catastrophizing
  • kinesiophobia
42
Q

how might IBS and centrally mediated abdominal pain (CAPs) be linked to the BPS-model?

A

IBS:
•Common chronic disorder believed to be an interplay of GI and neurogenic factors
•Strong link with anxiety, depression and/or stress
•Post gastroenteritis onset is common
•Clinical diagnosis is made after exclusion of ‘red flag’ conditions
•CBT may be used in addition to pharmacological
•Associated with stressful or traumatic events but conflicting evidence as to link with socioeconomic group
**Associated with altered bowel habits

CAPs:
•Presentation of pain without medical explanation with minimal motility disturbance
•Neuropathic-sensitisation with disinhibition of pain signal
•Onset often post GI insult or follows emotional stress
•Diagnosis clinical after ruling out other conditions
•Treatment with CBT, amitriptyline
**not associated with changes in bowel pattern or with another medical condition

43
Q

which of the following is suggested to be a nutritional factor associated with an increased risk of IBD?

a) Mediterranean diet
b) Westernisation of diet
c) Diet rich in fruit and veg
d) all of the above

A

b) westernisation of diet

44
Q

What factors contribute to the development of malnutrition in IBD and how can you reduce this risk?

A
  • Sweets, High fat, Low fibre, Alcohol, Vitamin D deficiency
  • Diet rich in fruits, veg, n3 fatty acid and low in n6 fatty acids
45
Q

Disease activity in IBD can lead to micronutrient losses (diarrhoea and inadequate dietary intake) leaving patients vulnerable to micronutrient deficiency. Patients with IBD should be checked for what micronutrient deficiencies on a regular basis?

A
  • Iron deficiency
  • Calcium and vitamin D (*higher risk of low bone density)
  • B12
  • Vitamin A
  • Folic acid
  • Zinc
46
Q

What nutritional screening tool is used to determine nutritional risk in patients with IBD?

A

MUST and management plan

Step 1 – BMI score
Step 2 - % unplanned weight loss
Step 3 – establish acute disease affect
Step 4 – add scores together to obtain overall risk 
Step 5 – use management guidelines
47
Q

what is coeliac disease?

A

systemic autoimmune (IgA)disease triggered by dietary gluten peptides (gliadin). affects the duodenum/ jejunum and leads to villous atrophy, hypertrophy of the intestinal crypts, and increased numbers of lymphocytes in the epithelium and lamina propria.

  • associated with epigastric pain, bloating, iron deficiency, worsening of symptoms after eating gluten, severe or occasional diarrhoea, tiredness, mouth ulcers
  • risk of osteoperosis, malignancy, ulcerative jejunitis
48
Q

what rash is associated with coeliac disease?

A

dermatitis herpetiformis - immune complexes cause irritation of the skin

49
Q

what recommendations would you give to a patient diagnosed with IBS?

A
  • regular meals
  • 8 cups of fluid
  • restrict tea and coffee
  • reduce alcohol intake and fizzy drinks
  • limit intake of high fibre
  • referral to dietitian
50
Q

list some causes of antibiotic resistance

A
  • over-prescribing
  • patients not finishing their course
  • poor infection control in hospitals
  • lack of new antibiotics being developed
51
Q

how would you treat ulcerative colitis and Crohn’s disease

A

UC:

  1. topical (rectal: proctitis or proctosigmoiditis) anti-inflammatory (5-ASA) or oral (left sided) depending on severity
  2. immune suppressant in severe disease (prednisolone)
    * *maintenance = 5-ASA

CD

  1. induce remission with steroid/immune suppressant
  2. anti-inflammatory for maintance
  3. immunomodulator (MABS) - third line for both

[not sure this is right!]

52
Q

what ways can pathogens become resistant to antibiotics?

A
  • Enzyme inactivation e.g. B-lactamases (chops up ring on AB chemical structure)
  • Enzymatic addition e.g. aminoglycosides (phosphorylate and inactivate)
  • impermeability e.g. B-lactams
  • Efflux e.g. tetracyclines (pump exists already, changing it slightly it will pump out AB)
  • Alternative pathway e.g. MRSA mecA (produces new type of peptidoglycan that bypasses block)
  • Altered target e.g. rifampicin (change binding site- single point mutation)
53
Q

how can resistance be countered

A
  • Phage therapy – natural and engineered viruses that attack and kill bacteria
  • Lysins – enzymes that directly and quickly act on bacteria
  • Antibodies – bind to bacteria or their products, restricting their ability to cause disease
  • Probiotics – prevent pathogenic bacteria colonising the gut
54
Q

What are the early symptoms for the 2 common types if infection in hospital?

A
  1. clostridium difficile: Significant diarrhoea, recent antibiotic exposure, abdominal pain, fever, foul stool odour
  2. MRSA: small bumps that look like pimples/boils, fever, widespread rash
55
Q

what patients are more at risk of infection?

A
  • Age more than 70 years
  • Shock
  • major trauma
  • Acute renal failure
  • Coma
  • Prior antibiotics
  • Mechanical ventilation
  • Drugs affecting the immune system (steroids, chemotherapy)
  • Indwelling catheters
  • Prolonged ICU stay (>3 days).
56
Q

what conditions causing abdominal pain would require urgent surgery?

A

perforations, haemorrhage, ischemia (including some hernias)

57
Q

what damage may occur as a result of gastrointestinal pathogens?

A
  • local inflammation
  • ulceration/perforation of mucosal epithelium(rupture of untreated ulcer)
  • disruption of normal microbiota (villous atrophy)
  • pharmacological action of bacterial toxins
  • invasion to blood or lymphatics
58
Q

bacterial diarrhoeal pathogen -Vibro cholerae

A
  • characteristic rice-watery stools (1L/hour)
  • rod shaped, flagellated
  • gram negative
  • flourished in communities with no fresh drinking water/ sewage disposal
  • infective in large quantities in small intestines
  • oral rehydration therapy crucial (hypovolemic shock)
59
Q

bacterial diarrhoeal pathogen - Escherichia coli

A

-rod shaped, pili/fimbriae
- gram negative
-different types: some possess virulence factors -> disease
-e.g. type EPEC responsible for sporadic cases and outbreaks in under 5s (enteropathogenic)
ETEC responsible for travellers diarrhoea (enterotoxigenic)
-2 mechanism that cause diarrhoea by heat-labile toxin increasing cAMP and heat-stable toxin increasing cGMP

60
Q

bacterial diarrhoeal pathogens - campylobacter jejuni

A
  • gram negative, helical bacillus
  • most common cause of diarrhoea in developed world**
  • in food e.g. consumption of undercooked meat
61
Q

bacterial diarrhoeal pathogens - salmonella

A
  • gram negative, bacilli
  • food-associated
  • secondary spread human-human
  • notifiable disease, can be chronic carrier!
  • 3 important species: S.typhi, S.paratyphi and S.enteritidis
  • absorption of epithelial cells in terminal small intestine. homes in on M cells in Peyers patches
  • systemic infection: enteric fever (typhoid and paratyphoid) multiple and transported in macrophages
62
Q

bacterial diarrhoeal pathogens - Shigella species

A
  • s.dysenteria is most serious
  • watery diarrhoea (pooy not rice water)
  • produce toxin
  • self-limiting
63
Q

pregnant women are advised to avoid foods such as pate, soft cheese, unpasteurised milk, humous. what bacterial pathogen is this to avoid?

A

listeria monocytogenes

64
Q

why might diarrhoea be a side affect of some antibiotic treatments?

A
  • antibiotic-associated diarrhoea doesn’t involve ingestion of pathogen or toxin
  • arises from disturbance of gut microbiota
  • e,g, tetracyclin allows colonisation by staphylococcus aureus and candida sp.
65
Q

what bacterial diarrhoeal pathogen produces spores for survival and is a major nosocomial infection problem?

A

Clostridium difficile

**hospital infections largely responsible for increase in cases

66
Q

what bacterial diarrhoeal pathogen multiplies in the large intestine, produces spores and enterotoxin?

A

food-associated GI infection - Clostridium perfringens

‘food-poisoning’

67
Q

what is the most common viral pathogen that causes diarrhoea in children (<2)?

A

rotavirus

-onset vomiting and diarrhoea lasting 4-7days

68
Q

what virus accounts for most non-bacterial outbreaks of diarrhoea

A

norovirus ‘winter vomiting virus’

  • no vaccine yet
  • avoid via hand washing!
69
Q

in what major way does protozoa and helminth infection differ from viral/bacterial infection?

A

usually chronic - can last years!

  • usually reflects levels of hygiene
  • more complex lifecycles
70
Q

what protozoal infection is also a cause of ‘traveller diarrhoea’ (like ETEC which is the bacterial cause)? what are the 2 stages of this pathogen?

A

Giardia lamblia -drinking and recreational water

1) trophozote - present in small intestine, sticks onto and damages brush boarder
2) cyst - resistant and pass out in stool

-‘stink-bomb stools’ because interferes with bile duct as well

71
Q

what is the protozoal cause of profuse and watery (25L/day!) diarrhoea that is usually self-limiting, but may become life-threatening in HIV +ve individuals? what is its lifecycle?

A

Cryptosporidium parvum

  • animal reservoir (cattle e.g. faeces in drinking water)
  • sexual and asexual lifecycles development in host
72
Q

what protozoa is produce cysts capable of infecting RBCs, after mucosal invasion, giving rise to amoebic colitis?

A

Entamoeba histolytica

73
Q

what are the most clinically important intestinal worms and give examples?

A

nematodes (roundworms):

  • soil-transmitted
  • diagnose with stool microscopy

eg1) strongyloides stercoralis:
- pinworm
- active skin penetration
- dysentery
- anal pruritic ‘itchy bum syndrome’
- associated with appendicitis

eg2) trichuris trichiura:
- whipworm
- infection from swallowing infective eggs on veg
- can live for 3yrs in gut

eg3) ascaris lumbricoides:
- giant roundworm (large, thick + white)
- adults live in gut for 2yrs
- ingested

eg4) enterobius vermicularis:
- threadworm
- females migrate to anus late at night to lay eggs
- intense itching

eg5) ancyclostoma duodenal:
- hookworm
- cause hypochronic anaemia by attaching onto small intestines, suck blood and protein

eg6) Taenia solium - tapeworm:
- ingesting eggs in undercooked pork
- reside in large int. 7m

Week 18: Abdominal Pain (2 decks)

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