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Year 2 > ILO WEEK 4 > Flashcards

ILO WEEK 4 Flashcards

1
Q

Diarrhoea

A

Normal stool weight is approx. 300g/24h
Volume greater than 200ml constitutes diarrhoea
More than 4 watery stools a day

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2
Q

Dystery

A

Bloody diarrhoea

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3
Q

Be able to recognize the duodenum, pancreas and spleen and give an account of the gross morphology and relationships.

A

look at professor McDonald picture ;D

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4
Q

Be able to name the parts of the duodenum and of the pancreas.

A

Duodenum:
Superior; Descending; Horiozontal; Ascending

Pancreas:
Head; Neck; Body; Tail

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5
Q

Appreciate the relationship between the bile duct, the head of the pancreas and the ducts of the pancreas and understand the anatomical arrangement of the common opening of the ducts into the duodenum.

A

Professor McDonald picture

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6
Q

Describe the anatomy of the portal vein and list the organs from which venous blood drains to it. Appreciate the functional significance of this arrangement.

A

blood from the gastrointestinal tract, gallbladder, pancreas and spleen to the liver

nutrients and toxins from digested contents

not an actual vein -> conducts blood to capillary bed instead of the heart
part of hepatic system

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7
Q

Describe the microscopical anatomy of the duodenum, pancreas and spleen and appreciate the ways in which their structure reflects their function.

A

!!!!!!

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8
Q

. Be able to give an account of portasystemic anastomoses and to describe their location and clinical importance.

A

a connection between the veins of the portal venous system, and the veins of the systemic venous system

Oesophageal – Between the oesophageal branch of the left gastric vein and the oesophageal tributaries to the azygous system.
Rectal – Between the superior rectal vein and the inferior rectal veins.
Retroperitoneal – Between the portal tributaries of the mesenteric veins and the retroperitoneal veins.
Paraumbilical – Between the portal veins of the liver and the veins of the anterior abdominal wall.

May cause varices, raptures, blood loss

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9
Q

Be able to recognize the duodenum, pancreas, spleen and portal vein on clinical imaging.

A

???

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10
Q

Understand the role of osmolality changes in determining water movement between intracellular and extracellular fluid, and the relevance of this to the treatment of fluid and electrolyte disorders.

A

d

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11
Q

Know main types of available intravenous fluids and their principal use.

A

Colloids (blood products) Albumin, hydroxyethyl starch (HES), Haemaccel; Large molecular weight
Crystalloids (water + electrolytes) saline, dextrose, ringer-lactate, Hartmann’s; Solution of electrolytes and water
Difference is that they stay in the vascular bed differently
Colloids stay for a while in the bed -> To fill vascular bed; acute haemorrhage
Glucose vanishes into the cells -> to rehydrate; gets into cells quickly; fluid leaves as well!; Clever way of giving water; cannot give clear water; with glucose water can be given to dilute extracellular fuid
Crystalloids -> saline stays longer than carbohydrates; patient that looks dehydrated but no acute shock Saline good to maintain the volume of vascular bed

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12
Q

Describe factors which determine the rate of fluid replacement.

A
  • Age
  • Cardiovascular status
  • Renal function
  • How much time it took for dehydration to develop
  • severity of dehydration
    -Always relate it to the individual patient!!!
    In patients with kidney failure -> may be lethal
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13
Q

Know the principles of safe potassium replacement.

A

maximum is 140mmol/24h

require 60-80 mmol a day normally

So should give: 80

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14
Q

Know cardiac effects of hypokalaemia and hyperkalaemia.

A

Related to risk of cardia arrhythmias

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15
Q

Develop a systematic approach to the assessment of a patient with suspected fluid/electrolyte disorder.

A

???

  1. Judge acid-base balance -> anion gap

    reference ~ 8-16

  2. Degree of renal insufficiency due to loss of blood volume; look at clinical signs of bleeding (Urea & Creatine); in older patients slightly increased creatine NORMAL
    
How we know kidneys are failing -> osmolality is normal range 
do urine to serum ratio
    
if less than 1.5 : 1 renal insufficiency
    

  3. HCO3- low -> ↓ due to diarrhoea or acidosis

The results could also suggest renal acidosis; however, history suggests diarrhoea

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16
Q

Describe the gross anatomy and histology of the large bowel including the anal canal

A

??? patrz extra kartki

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17
Q

Discuss the motility of the large intestine

A

Movement similar to small intestine but slower
Sluggish propulsory movements; short range of peristaltic waves in distal part

Haustrations (mixing movements) segmentations -> squeeze and roll
Mass movement -> several times a day; a vigorous propulsive movement of the colon; portion of the colon remains contracted for rather longer than during a peristaltic wave; emptying large portion of proximal end; initiated by intrinsic reflex pathways resulting from distention of the stomach and duodenum (Gastrocolic Reflex) 

Contractions controlled by parasympathetic nerve fibres

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18
Q

Explain the urea and electrolyte results in the scenario

A
  1. Judge acid-base balance -> anion gap
(Na+- [ Cl- + HCO3- ] ) reference ~ 8-16
Her results -> acidosis (result higher than reference)

  2. Degree of renal insufficiency due to loss of blood volume; look at clinical signs of bleeding (Urea & Creatine); in older patients slightly increased creatine NORMAL
How we know kidneys are failing -> osmolality is normal range 
do urine to serum ratio (her result -> 3:1)
if less than 1.5:1 renal insufficiency
    

  3. HCO3- low -> ↓ due to diarrhoea or acidosis

The results could also suggest renal acidosis; however, history suggests diarrhoea

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19
Q

Discuss the spread and control of enteric infection in healthcare settings

A
  • Wash hands with soap and water
  • Isolation of patients until symptom free for 48 hours
  • Using gloves
  • Disinfecting the surfaces
  • Stay off work if you have symptoms
    itditp

+

  • rotavirus and measles vaccinations
  • Early breastfeeding and it A supplementation
  • Improved water quality
  • community wide sanitation promotion
20
Q

Describe the factors affecting the motility of large intestine

A

Takes 1-2 days; men shorter than women


Reduce motility: opiates (μ receptors), anticholinergics, loperamide


Increase motility: laxatives, prucalopride (treats chronic constipation), linaclotide

21
Q

Investigations and treatment of diarrhoea

A

Treatment:
Fluid replacement therapy -> prevent dehydration (daily need; anticipated loss; previous deficit)
Usually isosmotic solutions to prevent electrolyte shift
Saline: dextrose 2:1
Potassium suplementation

Investigations:
Look out for:
- weight loss
- blood in stool
- evidence of dehydration
- nocturnal symptoms
- fever
- vomiting
- travelling, high risk group
- abdominal pain
- stress, anxiety

Do:

  • abdominal examination
  • rectal examination
22
Q

Role of SCFA in the colon

A
  • SCFA absorption is concentration dependent and occurs most readily in the proximal colon
  • Of the three SCFAs (acetate, propionate and butyrate) present within the colonic lumen, butyrate is the most important physiologically
  • Butyrate serves as a major source of energy for human colonocytes and plays a crucial role in colonocyte growth and differentiation
  • Butyrate produces a twofold increase in Na+ absorption
23
Q

urea:creatine ratio -> indications

A

If there is a GI bleeding then blood is digested like any other protein -> urea goes very high, creatine stays normal

24
Q

What increases insensible loss

A 
exercise 
sweating
fever
environment
dry air
skin burns
25
Q

PPD Previous day deficit=

A

(previous day measured losses+ Insensible losses)- previous day intake

26
Q

Fluid required measurement

A

PPD + ML + IL

27
Q

Liver function test findings

A

Chronic hepatitis- albumin would be decreased
Acute cholestasis- AST would be normal and ALP would be increased and albumin normal
Gilbert’s syndrome- unconjugated bilirubin would be increased
Primary biliary cirrhosis- ALP would be raised
Acute hepatitis -AST raised

28
Q

Inferior rectal artery

A

comes from internal pudendal artery

29
Q

Peyer’s Patches

A

Large aggregations of lymphoid tissue in the small intestine can be termed:

30
Q

Carbohydrates absorption

A

SGLT- glucose and galactose absorption
Na+/K+ ATPase- involved in establishing Na+ gradient for passive diffusion
Na+/H+ symporter- small peptide absorption
GLUT-2- all monosaccharides from cell to interstitial fluid
GLUT-5- fructose

31
Q

Campylobacter infection

A

Found in poultry and attach to and invade intestinal epithelial cells in small and large bowel. Causes symptoms as above as well as blood in stool. It is self-limiting and rarely needs antibiotics.

32
Q

Types of portal hypertension

A

Pre/post-hepatic - types of jaundice
Hepatic - example includes cirrhosis
Infra-hepatic - alterations to the PORTAL VENOUS blood flow

Budd-Chiari - hepatic vein thrombosis

33
Q

Understand the concept of water and electrolyte balance and identify the main processes which lead to fluid and electrolyte loss

A

The most important electrolytes:

Sodium (Na+) - the main ECF cation
Potassium (K+) - the main ICF cation
Chloride (Cl-) - the main ECF anion
Bicarbonate (HCO3-) - acid/ base balance
Calcium (Ca++) - main ECF anion 
Phosphate (P-) - the main ICF anion

Control of each is generally controlled by Osmolarity/ Osmolality. Osomolarity terms define the number of solute particles in 1L of solvent, Osmolality is the same but refers to 1Kg of solvent instead.

Sodium provides 50% of the osmotic pressure gradient between intra and extra cellular environments. Water will move passively between body compartments in response to the osmotic pressure gradients produced by “where the electrolytes are”.

Remember: other solutes, such as albumin and glucose will provide a “oncotic” pressure gradient.

Physiological mechanisms of fluid loss are mainly: insensible losses (such as sweat, respiration), exercise (sweating), D&V, alcohol in take. These will cause an upset in fluid/ electrolyte balance. Remember: water moves down gradient.

Management of this, and diarrhoeal causes are their own ILOs and will not be covered here.

34
Q

Identify the main electrolytes that may be lost through the gastrointestinal tract

A

Mainly Sodium (Hyponatremia), Potassium (Hypokalaemia) and Chloride (Hypochloremia).

35
Q

Understand the mechanism of intestinal transport of Glucose and apply this knowledge to the treatment of dehydration.

A

Why specifically glucose? I don’t really understand this.

It is co-transported with sodium into the cell via the SGLT1 Transporter on the apical face of the cell, and are transported by the GLUT2 Transported through the basal face by a gradient produced by NA+/K- ATPase which shuttles sodium out of the cell, and potassium in.

This discovery was key in the treatment of cholera with rehydration therapy. Not just replacing what is lost, but reducing what is lost. By reducing the solute content of Oral Rehydration Solution, but keeping Glucose constant stool output could be reduced.

36
Q

red blood cells in a patient with iron deficiency anaemia

A

Microcytosis and hypochromic (Smaller and paler)

37
Q

Classification systems for disease

A

Los Angeles = reflux oesophagitis
Marsh = coeliac
Prague = Barrett’s oesophagus
Duke’s = colorectal cancer

38
Q

Common bile duct pathway

A

Common bile duct passes :
-BEHIND duodenum
THROUGH the head of the pancreas
joins with main pancreatic duct
opens in to 2nd part of duodenum (Ampulla of Vater)
flow of bile regulated by Sphincter of Oddi (smooth muscle)

39
Q

Dermatitis Herpetiformis

A

Skin condition in coeliac disease

40
Q

Understand the mechanism of intestinal secretion of chloride ions and its role in the development of severe diarrhoea.

A

Water follows electrolytes.

Chloride, an anion, is secreted into the lumen of the intestines by enterocytes. This produces a -ve gradient that Sodium, a cation, then follows. Water then moves across this gradient due to osmolaric pressure. The result is the secretion of water and NaCl - salt.

This is regulated by the ion channel Cystic Fibrosis Transmembrance Conductance Regulator, CFTR, which is a cAMP dependant process.

Abnormal activation of CFTR, such as by enterotoxins produced by Vibrio Cholerae leads to secretory diarrhoea - high volume and watery.

41
Q

Know the basic classifications of diarrhoea and its main causes.

A

Acute, watery. - typically Secretory? - enteric infection
Acute, bloody. - typically Inflammatory? enteric infection/ IBD.
Persistent - lasting 14 days or more.

42
Q

Appreciate the importance of child diarrhoea as a public health problem world wide.

A

Infectious diarrhoea is often the sign of a self limiting infection, a prime example is cholera. It’s treatment is often simple: re-hydration. Even antibiotics in bacterial causes can be contraindicated.

Despite this, over 500,000 children a year die of diarrhoeal disease, which can often be blamed on unsafe water, poor sanitation, poor hygiene in poverty.

It can be prevented - wash hands, vaccinate, clean water.

43
Q

Describe fluid and electrolyte absorption

A

Sodium-

Absorbed three ways.

  1. Na-H antiporter on the apical surface.
  2. Epithelial sodium channels
  3. By symporters with short-chain fatty acids.

Chloride-

(and bicarbonate secretion) - the movement of sodium provides and electro-chemical gradient that also attracts chloride anions. Chloride is exchanged for bicarbonate.

Water-

Follows sodium.

Potassium-

Something of a physiological afterthought. The absorption/ secretion of the other ions provides the gradient for Potassium to then diffuse through membranes.

Regulated by Aldosterone (RAA) and Glucocorticoids.

Remember the lecture based specifics.

44
Q

Describe the pathogenic mechanism in diarrhoeal disease

A

Three main mechanisms. (verbatim from slides - this needs more detail!)

Toxin mediated - such as S.aurues, B.cereus, C.difficle, E.coli 0157.

Damage to the intestinal epithelial surface - C.difficile?

Invasion across intestinal epithelial barrier. - Salmonella

45
Q

Describe the normal flora (of the intestine)

A

Made up of over 200 species of bacteria, many of which are commensal. First introduced to the body by vaginal birth of the new born.

By far the most sophisticated and well researched is the gut flora. The proximal small intestine is mainly gram +ve, rich in lactobacilli and Enterococcus faecalis. The distal regions are far richer in microbiota in both CFUs and species.

In health, these can aid in immune defence and also digestions.

Benefits:

Provision of vitamins
Compete against pathogenic species
Can actively secrete bactericidal.static agents.
Aid to develop normal tissue such as Peyers Patches and the Caecum.
Stimulate the production of cross-reactive antibodies to allow immunity against pathogenic species.

Cons:

Pathogenic and commensal species can collude to allow infection, such as when normal flora staph shares drug resistance with pathogenic species.

Compete for nutrients

Induce toxaemia by the production of enterotoxin.

Can produce opportunistic infection

Can produce opportunistic infections in others

Implicated in cancer and autoimmunity.

Year 2 (8 decks)

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