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DMD2 > GASTROINTESTINAL TRACT > Flashcards

GASTROINTESTINAL TRACT Flashcards

1
Q

What are the 4 layers of the wall of the GIT?

A
  1. Mucosa
  2. Submucosa
  3. Muscularis Externa
  4. Serosa/Adventitia
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2
Q

How can you differentiate Adventitia from Serosa?

A

Serosa caintains simple squamous epithelium (mesothelium), loose CT, numerous adipocytes, nerves, blood and lymph vessels

Adventitia has NO epithelial layer

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3
Q

Which statement is incorrect regarding the histology of the Oesophagus

A. the mucosal layer of the oesophagus is stratified squamous epithelium
B. the submucosal layer has numerous glands and lymph nodules
C. the muscularis externa layer contains both striated and smooth muscle
D. the outermost layer contains epithelium, adipocytes, vessels and nerves

A

D - is incorrect

This statement is referring to a layer of Serosa which is not present in the oesophagus, the oesophagus has an outer layer of Adventitia

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4
Q

Match the cell to its secretion

Cells - Enteroendocrine, Chief, Parietal

A. Intrinsic factor and Hydrochloric acid
B. Histamine, Somatostatin, Substance P, Gastrin, Cholecystokinin and VIP
C. Pepsinogen

A

Parietal cells: Intrinsic factor and Hydrochloric acid

Enteroendocrine cells: Histamine, Somatostatin, Substance P, Gastrin, Cholecystokinin and VIP

Chief cells: Pepsinogen

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5
Q

What are the three key defence mechanisms of the gastric mucosa against acid?

A
  1. Luminal → Gastric mucus barrier
  2. Epithelial → Gastric epithelial cell barrier
  3. Mucosal Blood Flow → Underpins luminal and epithelial defences
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6
Q

Which is false about the gastric mucous barrier?
A. It is impermeable to pepsin
B. It allows ion movement
C. It is stimulated by prostaglandins
D. Bicarbonate is secreted by surface mucous cells

A

B is false - Impedes ion movement to prevent backflow of H+ to the cell

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7
Q

What are the three mechanisms of protection by the gastric epithelial cell barrier against acid?

A
  • Tight Junctions between surface cells → Prevent H+ diffusing between cells
  • Active transporters on cell membranes → H+ and HCO - transport
  • Rapid healing of gastric mucosal cells
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8
Q

Distinguish cytoprotection and adaptive cytoprotection.

A
  • Cytoprotection = Prevention of tissue damage from noxious agents by prostaglandins
  • Adaptive cytoprotection = Exposure to mild irritants stimulates prostaglandin release which prevents further damage
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9
Q

Define peptic ulcer and distinguish from erosion.

A

o Ulcer = Damage to full thickness of mucosa and into submucosa; wider and deeper than erosion (breadth >3mm and depth)
o Erosion = Damage superficial to submucosa

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10
Q

Which is most correct in relation to NSAIDs?
A. Inhibits COX1 pathway to prevent inflammation and pain
B. Non-selective NSAIDS have high CVD complications
C. NSAID-associated ulcers are generally silent
D. Most common side effective is enhanced GFR and inhibition of tubular sodium reabsorption

A

C is most correct

A. Referring to COX2
B. Referring to COX2 selective NSAIDs
D. Correct but is is not the most common side effect - GIT disturbances are most common.

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11
Q

List some products release by helicobacter pylori that result in inflammation of GIT.

A
  • Mucinase → Degrades mucus glycoproteins
  • Platelet-activating factor → Injures mucosa and creates thrombosis
  • Phospholipase → Damages epithelial cells
  • Cytotoxins → Injures mucosa and influence inflammation
  • Upregulates gastrins → ↑ Acid output
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12
Q

What is the first line of treatment for peptic ulcer?

A

First-line eradication therapy (3 components):

  • Proton pump inhibitor
  • Amoxicillin 1g
  • Clarithromycin 500mg (low abx resistant)
  • All 2x daily for 7 days
  • Note: Secondary resistant is high in patients with first line resistance → Avoid repeating if failure.

Aim to eradicate h.pylori with abx first and then PPI and H2 receptor agonists may be used to inhibit acid secretion.

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13
Q

What are the three main gut motility phenomena?

A

o Contractile activity and tone
- Phasic contractions = Brief periods of contraction and relaxation (e.g. peristalsis)
- Tonal contractions = Long duration contractions (e.g. sphincters)
o Flow and transit: Time required for lumen contents to travel through a region of the gut
o Compliance: Capability of GIT to adapt to an imposed intraluminal pressure (stretch and change size in response to content)

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14
Q

Which of the following is true in regards to organs and sphincters in gut motility?
A. Pyloric is between the oesophagus and stomach
B. Large intestine is involved in propulsion, storage and mixing
C. Illeo-cecal is between the ileum and stomach
D. Oeseophagus is involved in propulsion and storage

A

B is true

A. Pyloric is between stomach and small intestine
C. Illeo-cecal is between ileum and the large intestine
D. Oesophagus involved in propulsion only

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15
Q

Distinguish between primary and secondary oesophageal peristalsis.

A
  • Primary → Response to swallowing

- Secondary → Reflex to clear oesophagus (purpose to expel remnants)

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16
Q

Distinguish between the two types of digestive patterns in small intestine motility.

A
  1. Inter-digestive motor activity
    - Migrative motor complex (ENS) stimulates movement
    - Purpose of MMC to grind down remnants in stomach
    - Activated in fasting state
  2. Digestive motor pattern → Vagally stimulated mixing
    - Activated in fed state
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17
Q

What are the three types of signalling in enteric nervous system?

A

o Neuron to Neuron – e.g. ACh, 5-HT, Substance P, NE
o Endocrine – e.g. CCK and Gastrin
o Paracrine – e.g. 5-HT, histamine, cytokines

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18
Q

Describe the vomit reflex sequence.

A

• Vomit reflex sequence:
o Reverse contraction from jejunum and ileum to duodenum
o Opening of pyloric sphincter
o Intestinal contents travel into stomach
o Inspiration with glottis close to decrease intrathoracic pressure
o Lowering of diaphragm to increase abdominal pressure
o Opening of lower oesophageal sphincter
o Abdominal muscle contraction pushes stomach contents into oesophagus
o Opening of upper oesophageal sphincter
o Gastric antrum contract expels contents from mouth
o Peristalsis sweeps oesophageal contents back into stomach

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19
Q

Which of these statements regarding disordered oesophageal motility is most correct

A. Achalasia is the absence of primary peristalsis with failure of LOS activation
B. Diffuse oesophageal spasms result in heartburn
C. Reflux is a transient inappropriate activation of LOS
D. non-peristaltic high amplitude contractions result in chest pain

A

D is correct - this is referring to diffuse oesophageal spasm

A - incorrect, the failure is of LOS relaxation not activation
B - incorrect, this results in chest pain
C - incorrect, again its an inappropriate lack of LOS relaxation not activation

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20
Q

What is the defining feature that distinguishes dyspepsia from GORD?

A

Epigastric pain >/= 1 month in dyspepsia

Note: There are overlapping symptoms such as heartburn and reflux in both.

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21
Q

Explain the three ways to test for H.Pylori

A
  • Serology test - convenient, less expensive but false +/- (never conclusive, rarely used now - need other tests to confirm)
  • Faecal antigen test
  • Urea breath test - Test of choice due to high sensitivity and specificity, non invasive.
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22
Q

List 5 alarm symptoms that trigger referral to specialist in relation to dyspepsia.

A

• Alarm symptoms and triggers for referral
o Older patients >55 with new onset symptoms
o Unexplained weight loss > 10%
o Severe debilitating pain
o Persistent vomiting
o Referred pain
o Anorexia
o Anaemia – GIT blood loss
o Melaena (dark sticky stools) – related to upper GIT (time to oxidise by the time it is excreted)
o Dysphagia (difficulty swallowing)
o Haematemesis (blood in vomit)

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23
Q

Which of the following is true?
A. Haematemesis most likely indicates gastric and oesophageal cancers
B. Dyspepsia is defined as pain below the umbilicus
C. Peptic ulcer pain is relieved by food
D. Bloating and flatulence are symptoms of GORD

A

C is true.

A. Most likely indicates functional dyspepsia. Gastric and oesophageal cancers are very unlikely indicated in haematemesis.
B. Defined as pain ABOVE umbilicus.
D. Symptoms of dyspepsia.

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24
Q

What non pharmacological management of dyspepsia can be undertaken?

A

o Adjusting or stopping drugs that cause symptoms
o Avoid alcohol, coffee and smoking (or any other triggers)
o Reducing weight
o Reducing meal size (small frequent meals)
o Drinking fluids between meals rather than with meals
o Avoid eating 2 to 3 hours before bedtime or vigorous exercise
o Elevate the head of the bed (night symptoms) before

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25
Q

Briefly explain the MOA of PPIs and H2 antagonists. Which one is more potent and why?

A 
CO2 + H2O ⇋ H2CO3. ⇋ HCO3 + H+
- Bicarbonate is exchanged for chloride
CO2 and H2O from blood converted for carbonic acid and then broken down into bicarbonate and hydrogen ion. 
- Process mediated by CA. 
- Proton comes from this equation

H+K ATPase pump out Protons (H+) and Chloride channels pump out Chloride ions: H+ + Cl- → HCl

  • Proton goes into the stomach lumen
  • PPIs work at this point to block HCl production

When we eat, distention → Gastrin → Stimulate enterochromaffin-like cells release histamine → Stimulates acid secretion (fuels H+K ATPase pump)

  • H2 antagonists block histamine activity and therefore less acid
  • Not as potent as shutting down the entire pump (ie. PPIs)
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26
Q

Which is false?
A. H2 antagonists side effects include confusion, rash, hypersensitivity reactions,
B. PPIs are best taken 30 - 60 minutes before a meal
C. Precautions should be taken for patients with renal impairment and heart failure risk when prescribing antacids
D. Antibiotics are recommended for functional dyspepsia

A

D is false. Antibiotics only used for H.Pylori associated dyspepsia

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27
Q

When is an endoscopy recommended with onset of dyspepsia?

A

Age >/= 60

Alarm features

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28
Q

What is the recommended triple therapy for H.Pylori associated dyspepsia? (assuming no allergies)

A

PPO, clarithromycin, amoxicillin - 7 day regimen.

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29
Q

What are the four components of the epithelium which protect against invading pathogens and ensure tolerance against commensal bacteria?

A
  1. Goblet cells - mucous secretion
  2. Paneth cells - antimicrobial peptide production
    - producing defensins which limit microbial load in the lumin, ther are alpha (in small intestine) and beta (in colon) subtypes
  3. Microfold cells - transcellular transport from the lumen to APC’s in the Peyers Patches
  4. Tight Junctions - forming the physical barrier
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30
Q

Which of the following regarding GIT immunity is incorrect

A. Luminal antigens can be taken up by transcytosis through M cells
B. Epithelial cell TLR’s are only present on the basolateral side of the cell to avoid commensal mediated inflammation
C. CD4+ cells are found predominantly in the lamina propria
D. T-regulatory cell differentiation is mediated by the conversion of vitamin A to TGF-beta

A

Answer D.
Induction of T-regulatory cells is via the conversion of vitamin A to retinoic acid (via dendritic cells). The retinoic acid then binds to TGF-beta for induce the naiive T-cells into T-regulatory cells

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31
Q

What are four outcomes of dysregulation in the immunity of the gut

A
  1. Inflammatory bowel diseases
    - abnormal Th1 and Th17 responses, defective function of Tregs, defective defensins or inability of innate cells
  2. Coeliac Disease
    - abnormal CD4+ response to gliadin - leading to an inflammation in the small intestine
  3. Food allergies
    - abnormal Th2 immune response to food antigens
  4. Tumours
    - due to prolonged immune response to commensal bacteria
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32
Q

Which of the following statements regarding GIT secretion and absorption is most correct?

A. Cl- channels are Ca+ mediated
B. DRA is a Cl-, H+ exchanger
C. The distal colon and rectal epithelium contain DRA and ENaC channels
D. The distal colon and rectal epithelium have ion flow paracellularly

A

C is correct

A - Cl- channels are CFTR, mediated by cAMP
B - DRA is a Cl-, HCO-3 exchanger
D - Distal colon and rectal epithelium have electrically tight junctions therefore have 0 ion flow paracellularly

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33
Q

Discuss the 3 phases of gastric acid secretion

A
  1. Cephalic phase
    - the thought, taste, smell, chewing and/or swallowing of food stimulates the vagus nerve to activate parietal and G-cells via ACh and Gastrin
  2. Gastric phase
    - distension of the stomach stimulates local enteric and vasovagal reflexes to secrete ACh and Gastrin which activate parietal and G-cells
  3. Intestinal Phase
    - protein digestion products in the duodenum and duodenal distension stimulate enteroendocrine cells via CCK and then inhibit secretion via the vasovagal path using secretin, GLP-1 and PYY
34
Q

Define diarrhoea

A

Frequent stools (>3/day) and/or Altered/decreased consistency of stools

35
Q

Which of the following statements regarding diarrhoea is correct

A. Osmotic diarrhoea is due to an increased load in the lumen which draws fluid in, does not resolve on fasting

B. Secretory diarrhoea is usually related to IBD and infections

C. Small bowel diarrhoea has blood and mucous inclusions and audible gurgling sounds

D. Large bowel diarrhoea is usually a large volume and is often related to colitis (ulcerative/ischaemic)

A

B is correct

A - this is mostly correct except it DOES resolve on fasting

C - small bowel diarrhoea does NOT have blood and mucous, this would be more likely found in large bowel diarrhoea

D - this is mostly correct except that its a smaller volume not a large volume

36
Q

List 4 common causes of diarrhoea

A 
IBS
Bile acid
Dietary (FODMAP, lactase deficiency, excess alcohol etc.)
Colonic neoplasia
IBD
Coealiac disease
Drugs (AB's, NSAIDs, Magnesium etc.)
Overflow diarrhoea
37
Q

Define coeliac disease

A

Coeliac disease is an immunologically mediated disorder of the small intestine caused by dietary exposure to triggering proteins in wheat, barley and rye

38
Q

Which statement regarding coeliac disease is incorrect

A - individuals with coeliac disease will have HLA DQ2/8, but individuals with HLA DQ2/8 will not necessarily have coeliac disease

B - HLA DQ2 accounts for >90% of coeliacs

C- tissue transglutaminase is central to the immune response in coeliac disease. In health there is limited-no antibody presence

D - The complete digestion of gliadins and presentation of the gliadin-tTG complex to CD8+ T cells are two steps involved in the pathogenesis of coeliac disease

A

D is incorrect
- incomplete digestion of gliadins and then concurrent gliadin-tTG complex presentation to CD4+ T cells that plays a role in the pathogenesis

39
Q

List 3 investigations for diagnosing coeliac disease

A

Antibody testing
Small bowel biopsy
HLA testing (adjunct)

40
Q

Define IBS and discuss its clinical features

A

IBS is a functional disorder of the GIT characterised by chronic abdominal pain and altered bowel habits

Clinical Features

  • abdominal pain
  • altered bowel habits (diarrhoea, constipation or alternating)
  • bloating
  • flatulence
41
Q

Define failure to thrive (absolute and relative)

A

Absolute - attained growth
where weight is <3rd centile, height <5th centile and/or weight is <20% of the ideal height:weight ratio

Relative - relative rate of growth
Where there is a fall from the previous growth curve of equal to or more than 2 centiles

42
Q

Which of the following is not an aetiological factor underlying the failure to thrive

A - inadequate intake
B - decreased absorption
C - excessive losses
D - abnormal utilisation
E - decreased need
A

Answer - E

It isnt a decreased need but rather an increased need
e.g. due to neoplasms, congenital heart disease or chronic illness causing an imbalance of requirement/expenditure that leads to the failure to thrive

43
Q

What are 4 psychosocial factors affecting child growth?

A

Any of the below;

  1. carer preoccupation with own issues (post natal depression)
  2. carer external demands (large families)
  3. drug/alcohol abuse
  4. poverty
  5. domestic violence
  6. absence of support
  7. lack of parenting support
  8. parental intellectual disability
44
Q

List the common viral infections of the GIT

A

Rotavirus, cytomegalocirus (CMV), norovirus

45
Q

Which of the options below is not a common bacterial cause of GIT infection

A. Giardia
B. E.coli
C. H.pylori
D. Shigella
E. Clostridium
A

Answer - A

Giardia is a parasitic infection of the GIT

46
Q

What are the common transmission routes of GIT infections

A

Faecal-oral, waterbourne/contaminated water, person-person

47
Q

Briefly explain how fats are digested.

A
  • Attack by gastric lipase and bile emulsifies large fat droplets
  • Pancreatic enzymes (pancreatic lipase - require colipase) breakdown TAGs to monoglycerides and FFA
  • Bile salts form micells = Hydrophobic core and hydrophillic surface
  • Micelles fuse with the enterocytes
  • Brush border enzymes (phospholipase, sphingomyelinase) break down micelle
  • Monoglycerides and FFA reconsittutded into chylomicrons for transport to lymphatic system for circulation OR small chain TAGS can bypass system and enter portal venous system
48
Q

Which of the following is false?
A. Vitamin B12 binds to intrinsic factor from parietal cells for absorption in SI
B. Iron absorption occurs in illeum
C. Glucose and galactose are transported through apical membrane of SI via SGLT1
D. Absorption of water in SI primarily driven by Na+ and glucose transport into enterocytes (drives osmotic gradient)

A

B. Iron absorption occurs in duodenum

49
Q

What are the four phases of pancreatic secretion?

A 
1. Basal secretion → Interdigestive period 
	Maximal during MMC 
2. Cephalic phase → Sight, smell, taste of food 
	20-25% maximal 
	Mainly acinar in origin
	Mediated by vagus → Ach (+VIP)
3. Gastric phase → Antral distension
	10% maximal 
	Mainly acinar in origin
	Mediated by vagus → Ach
4. Intestinal phase → Presence of H+, aromatic L-amino acids, peptides and fatty acids in lumen 
	50-80% maximal 
	Ductal and acinar in origin 
	Mediated by Secretin (H+) and CCK
50
Q

Explain function of maltase, lactase and sucrase.

A

Maltase → Breaks down maltose to glucose
Lactase → Breaks down lactose to glucose and galactose
Sucrase → Breaks down sucrose to glucose and fructose

51
Q

Which of the following is false?
A. S cells produce secretin which stimulates HCO3 secretion from bile ducts and pancreatic acini secretion
B. I cells produce CKK to stimulate HCO2 secretion via pancreatic ducts and gallbladder contraction for secretion of bile
C. Gastrin stimulates chief cells to release HCl
D. Somatostatin inhibits production of HCl, secretin, histamine and gastrin.

A

C. Gastrin stimulate PARIETAL cells to release HCl which CHIEF cells release pepsinogen

52
Q

What can distinguish fat malabsorption and fat maldigestion in assessment of fatty stools?

A

Fat malabsorption = Polarising crystals

Fat maldigestion = Globules of fat

53
Q

Distinguish ulcerative colitis and Crohn’s disease based on location and histological appearance.

A

UC = Confined to the colon, begins in rectum and travels upwards.

  • Mucosa and submucosa inflammation that is CONTINUOUS
  • Superficial ulcers
  • Rarely strictures and no granulomas

CD = Entire GIT can be affected

  • Transmural inflammation that is DISCONTINUOUS
  • Deep ulcers and fissures
  • Strictures and granulomas
  • Fistulae
  • Cobblestone mucosa
54
Q

Which of the following is true?
A. Ulcerative colitis is rarely associated with bleeding
B. Crohn’s disease ay have oral manifestations of mucosal tag lesions and lip hypertrophy
C. 5-aminosalicylic acid is used to treat Crohn’s disease
D. Smoking is a risk factor for ulcerative colitis

A

B is true.

A. UC commonly associated with bleeding
C. False as shown to be ineffective in CD (used in UC instead)
D. False as non-smokers showed higher risk than ex-smokers for UC

55
Q

Explain mechanism of diarrhoea caused by rotavirus.

A

 Infection/destruction of villi tips
 Repopulated by immature secretory cells = Decreased functional capacity (lack of absorption in small intestine)
 Osmotic diarrhoea from incompletely absorbed nutrients

56
Q

What are 3 key primary functions of liver?

A

o Bile production and excretion
o Metabolism of fats, proteins, and carbohydrates
o Glycogen synthesis and storage
o Synthesis of clotting factors and plasma proteins (prothrombin is ONLY produced in liver)
o Blood detoxification

57
Q

Which of the following is false in regards to liver structure and anatomy?
A. Located in abdominal cavity deep to thoracic cage
B. Dual blood supply from hepatic artery and portal vein
C. Diaphragmatic surface contacts gastrointestinal structures
D. Right side is larger

A

C is false as diaphragmatic surface only contacts diaphragm

58
Q

What is the role of kupffer, ito and pit cells? Name their location.

A

• Kupffer Cells:
o Phagocytic cells that form lining of sinusoids in liver
o Function – Phagocytosis of bacteria/virus, debris, RBCs, protein complexes

• Ito Cells:
o Also called Perisinusoidal cells or Hepatic stellate cells
o Found in perisinusoidal space (just outside sinusoids)
o Function – Secrete collagen in response to tissue damage, leading to fibrotic cirrhosis

• Pit Cells:
o Found in perisinusoidal space
o Function – Natural killer cells of liver

59
Q

Which of the following is true in regards to liver function tests?
A. Elevated ALP definitely indicates liver disease
B. Serum albumin is elevated in chronic liver disease
C. Vitamin K is low in liver disease as it is produced by the liver
D. AST is more elevated than ALT in alcoholic hepatitis

A

D is true.

The below are false due to
A. ALP is also contained in the bone and intestine. Elevated GGT in combination with elevated ALP can indicate liver disease.
B. Serum albumin produced in liver and therefore decreased in chronic liver disease
C. Vitamin K is low due to low bile (produced by liver) which is required for absorption of Vitamin K from diet (Vit. K is fat soluble)

60
Q

What are the four key symptoms of metabolic syndrome?

A

o Central adiposity
o Dyslipidaemia
o Abnormal blood glucose OR insulin resistance (i.e. Pre-diabetes)
o Hypertension

61
Q

Distinguish NAFL and NASH.

A

Non-alcoholic Fatty Liver (NAFL) = Hepatic steatosis with NO hepatocyte injury. (nil inflammation). Also called “Simple Steatosis”

Non-alcoholic Steatohepatitis (NASH) = Hepatic steatosis with hepatocyte ballooning, inflammation, and fibrosis → May progress to cirrhosis

62
Q

What are secondary causes of hepatic steatosis - name three.

A
  • Excessive alcohol consumption
  • Hepatitis C
  • Medications (e.g. methotrexate, corticosteroids)
  • Starvation
  • Lipodystrophy
63
Q

What are 3 of the most predictive signs of significant dehydration in children

A

Respiration - tachypnoea
Capillary refill - prolonged (>2seconds)
Skin turgor - recoil 2 seconds or greater

64
Q

Which of the options below is not an antidiarrhoeal?
- discuss the MOA of antidiarrhoeals

A. codeine
B. diphenoxylate
C. loperamide
D. Promethazine

A

Answer D –> this is an antihistamine

MOA of anti-diarrhoeals: activating opioid receptors on the GI wall decreases motility and hence increases fluid absorption.

65
Q

List 2 examples each for acute and chronic causes of vomiting/nausea

A

Acute: food poisoning, motion sickness, alcohol excess, pregnancy, chemo, post-operation, head injury, acute abdominal injury, diabetic ketoacidosis

Chronic: mechanical obstruction, untreated reflux, peritoneal inflammation, cancer, metabolic/endocrine disorder (diabetes, thyroid), medications, gastroparesis, neurological disorder (migraine, parkinsons), anxiety/depression

66
Q

Which of the following is true about antiemetics?

A. If a patient does not respond to an antiemetic, the best route is to increase the dose
B. no antiemetic works on all receptors (none are universally effective)
C. causes of nausea and vomiting are primarily related to effects on dopamine
D. oral is the only route of administration for antiemetics

A

Answer B

Incorrect
A - the best route is to try another antiemetic with a different MOA
C - there are numerous different causes of nausea and vomiting, all havying varying effects on DA, 5HT, H1, cholinergic and NK1 pathways (hence why the above is effective)
D - antiemetics can be given orally, rectally or parenterally

67
Q

Which of the following statements is the most correct

A. Hepatitis A and E are acute infections which can become chronic
B. All hepatitis viruses are ssRNA
C. Hepatitis D requires Hepatitis B to form its surface antigens
D. Hepatitis E and Hepatitis C currently do not have vaccines

A

Answer - D

Incorrect
A - E can have lead to chronic infection in immunosuppressed patients but A is only ever an acute infection
B - No, Hep B is a partially dsDNA virus
C - Hep D does require Hep B but this is to form the envelope, not the surface antigens

68
Q

Briefly discuss the serology of Hepatitis B

A

Where the HBsAg (surface antigen) is +ve, the patient may have an acute or chronic infection

  • If its acute they will also have the presence of IgM
  • If its chronic they will not be +ve for IgM
Where HBsAg (surface antigen) is -ve the patient could be susceptible, recovered/resolved HepB or vaccinated
- If they are succeptible they will be -ve for both anti-HBs and anti-HBc
  • HBc - core antigen and HBs - surface antigen
  • If they are +ve for both anti-HBs and anti-HBc, this means they have a resolved HepB infection
  • they have antibodies to both the surface and the core antigens
  • If they are +ve for only the anti-HBs the patient has been vaccinated
  • as the vaccine is an inactive form there was no replication and therefore no exposure of the core antigen - hence the vaccinated are only immunised against the surface antigen
69
Q

List the clinical features of liver failure (including those in decompenstated liver failure)

A 
Malnutrition (muscle wasting, loss of fat deposits, thinning of the skin)
Spider Naevi
Palmar Erythema
Scratch Marks
Hyperpigmentation
Feminisation in males

Decompensation
Fluid retention –> ascites, peripheral oedema
Jaundice & excessive bruising

70
Q

What is the pathogenesis of ascites

A

3 components
1. portal hypertension leads to splanchnic vasodilation –> decreased blood vol –> RAAS –> Na and H20 retention–> inadequate compensation –> more Na and H20 retention –> ascites

  1. portal hypertension leading to splanchnic vasodilation –> increases splanchnic capillary pressires –> lymph production outweighs return –> fluid build up –> ascites
  2. decreased albumin –> ascites
71
Q

Define hepatorenal syndrome

A

progressive renal failure assoc. w/ advanced cirrhosis and ascites

  • gradual rise in creatinine, and urine output failure
  • NIL intrinsic renal disease
  • exclusion of other causes
72
Q

Which of the following statements is the most correct

A. all upper GI bleeds are associated with varices
B. portal hypertension leads to an increase in oesophageal vasculature, these vessels are thin walled and hence they expand and cause obstruction
C. oesophageal varices are a major life threatening complication
D. presence of cirrhosis and liver disease are poor predictors of variceal bleeding risk

A

Answer - C

Incorrect
A. only 50% of those with a GI bleed and cirrhosis are due to varices, may others can be related to peptic ulcer gisease, coagulopathies etc.

B. this is mostly correct though the thin walled vasculature does not cause obstruction but rather expands and ruptures –> variceal bleeding

D. These are good predictors of risk

73
Q

List haemostatic disorders in liver disease

A 
platelet disorders
decreased synthesis of coagulation factors
vit-K deficiency-related coagulopathy
dysfibrinogenaemia
fibrinolysis
DIC
74
Q

Which of the following statements is incorrect

A. bone disease in cirrhosis is due to reduced bone formation and turnover
B. Malnutrition in cirrhosis is due numerous factors including; malabsorption, insulin resistance, decreased protein synthesis
C. Alcohol has a direct effect on bone metabolism
D. An accurate assessment of malnutrition can be made in patients with liver disease

A

Answer D - an accurate assessment is difficult to make in these patients because of fluid retention and hypoproteinaemia

75
Q

What are the three causes of jaundice?

A

o Pre-Hepatic = Pathology occurring prior to liver (with normal liver function)
 Increased haemolysis
 Neonatal jaundice – Due to breakdown of foetal Hb for replacement, and immature liver metabolism

o	Hepatocellular = Pathology occurring within liver due to diseased hepatocytes, resulting in cell necrosis or defective bilirubin metabolism
	Acute
•	Viral hepatitis
•	Hepatoxic drugs – e.g. alcohol, paracetamol
	Chronic
•	Viral hepatitis
•	Autoimmune hepatitis
•	Wilson’s disease
•	ALD and NAFLD

o Post-Hepatic = Pathology occurring after conjugation of bilirubin in liver, due to obstruction of bile duct and canaliculi
 Malignancy
 Gallstone

76
Q

Which of the following is false?
A. HAV mainly spread faecal-orally
B. Treatment for HCV involves antiviral therapy that can successfully eradicate the virus.
C. HEV may cause chronic illness in immunocompromised patients.
D. Acute, past and chronic infection of HCV can be distinguished through serology test.

A

D. Require HCV-RNA
Acute = Positive
Past = Negative
Chronic = Positive - can look at erratic elevations of ALT and signs of liver failure to distinguish from acute

77
Q

Briefly explain the three steps of metabolising alcohol (major oxidative pathway) in low/normal consumption

A
  1. Oxidising ethanol to acetaldehyde –> Mediated by alcohol dehydrogenase (MEOS - CYP450 mainly in chronic high consumption)
  2. Aldehyde dehydrogenase oxidising acetaldehyde to acetic acid
  3. Acetic acid converted to acetyl coa and into citric acid cycle
78
Q

Define cirrhosis and briefly explain pathogenesis

A

Cirrhosis = Extensive fibrosis and regenerative nodules disrupt the normal architecture of liver

Pathogenesis:

  1. Hepatotoxins or Immune response (e.g. HBV)
  2. Hepatocyte and connective tissue destruction
  3. Activation of Ito cells
  4. Fibrosis of ECM
  5. Nodular regeneration of remaining liver parenchyma
79
Q

Which of the following is false in regards to cirrhosis?
A. All chronic liver diseases may lead to cirrhosis
B. Ascites results from portal hypertension and may be managed with diuretics
C. HAV is a common cause of cirrhosis
D. Hepatic encephalopathy is generally reversible.

A

C. is false.

HBV and HCV are the most common viral hepatitis to result in cirrhosis and HCC

80
Q

What are the 3 main broad concerns for the clinical team when treating a patient with liver disease

A
  1. Liver metabolism –> impairment will affect the clearance of medications, also best to decrease doses of hepatotoxic medications
  2. Bleeding tendencies –> there is a likelihood that a patient with liver disease will also have coagulopathies or thrombocytopaenia
  3. Transmission of hepatitis viruses (most specifically HCV as there is no immunisation for this) –> adequate sterilisation protocols MUST be implemented and followed
81
Q

Which of the following statements is the most correct

A. A cellular example of tolerance is the phosphorylation of G-coupled receptors in Opioid use resulting in opioid receptor upregulation
B. Withdrawal symptoms are due to a decreased number of receptors
C. Addictive drugs are all able to activate the mesocorticolimbic system, resulting in a release of dopamine
D. Counteradaptive changes are not associated with withdrawal

A

C is correct

A - this is almost true, though it results in downregualtion of the receptors

B and D- withdrawal is not really associated with the receptors but rather with counteradaptive changes, ie. upregulation of cAMP in benzodiazepine use so that when the drug is ceased a higher than normal level of cAMP is still produced and the patient then suffers the effects (anxiety, insomnia etc. - opposite effects to the drug)

82
Q

Define substance use disorder

A

as per DSM-V
11 criteria, should you fulfil 2-3 (mild), 4-5 (moderate) or 6-7 (severe)

criteria included;

large amounts/longer time used
inability to quit
increased time obtaining substance
craving
tolerance
withdrawal
recurrent/consistent use
decreases in social activity
unable to carry out obligations due to use
continued use in the face of persistent social problems caused by use

DMD2 (13 decks)

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