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PBL Y2 S4 > Case 3- Pancreatitis > Flashcards

Case 3- Pancreatitis Flashcards

1
Q

What ducts lead into the main pancreatic duct?

A

Intralobular ducts

i.e., Acini within the exocrine pancreas are connected by intercalated ducts. These ducts unit with lobules to form intralobular ducts, which then flow into the main pancreatic duct

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2
Q

What cell types are present in the pancreas and what do they secrete?

A

Alpha cells - glucagon
Beta cells - insulin and amylin
Delta cells - somatostatin
Gamma cells - pancreatic polypeptide
Epsilon cells - ghrelin

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3
Q

What is the role of:
- Amylin
- Pancreatic polypeptide
- Ghrelin

A

Amylin = slows gastric emptying to prevent a spike in blood glucose
PP= Gi function
Ghrelin = increases appetite

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4
Q

What does release of glucagon lead to?

A
  • Increased glycogenolysis
  • Decreased glycogenesis
  • Increased gluconeogenesis
  • Increased ketogenesis
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5
Q

Where are digestive enzymes stored in the pancreas?

A

Within zymogen granules in acinar cells

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6
Q

What enzymes does the pancreas secrete and what do they digest?

A
  • Proteases = chymotripsinogen and trypsinogen, digests proteins and peptides into AAs
  • Pancreatic lipase = digests triglycerides, monoglycerides and free FA
  • Amylase= digests starch and maltose (dissacharides)
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7
Q

How is bicarbonate secreted?

A
  • H2O and CO2 combine in pancreatic ductal cells to form carbonic acid, which dissociates to HCO3- and H+
  • H+ is exchanged into the blood for Na+ (via antiporter), then Na+ goes back into the blood via Na+/K+ ATPase
  • HCO3- is exchanged for Cl- and enters into lumen of intercalated ducts of pancreas
  • HCO3-, Na+ and H2O move through intercalated ducts and enter main pancreatic duct
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8
Q

What increases pancreatic juice secretion?

A
  • Vagal innervation (PNS): i.e. sight, smell, taste of food or stretched stomach
  • CCK: released by I cells in response to FA and protein content within chyme in the duodenum (also causes bile secretion via gall bladder contraction)
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9
Q

What stimulates bicarbonate secretion?

A

Secretion - acidic chyme in duodenum stimulates S cells to release secretin, which causes ductile cells to secrete HCO3-, lowers bile secretion and inhibits gut motility

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10
Q

What does the ileum absorb?

A

Vitamin B12, bile salts and K+

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11
Q

What does the colon absorb?

A

Na+, some water, and short-chain fatty acids

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12
Q

What are 2 important features of the small intestine?

A
  • Expansion of absorptive surface: achieved by foldings in the wall, villi and microvilli
  • Polarised expression of transport proteins, i.e. different ones on different sides of the cell
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13
Q

What is secondary active transport?

A

Transport against a concentration gradient, with energy derived from Na+ gradient from the Na+/K+ ATPase (primary active transport)

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14
Q

What transporter is present on the apical membrane of the gut lumen for glucose or galactose absorption?

A

SGLT1: an Na+ dependent (secondary active) transporter; brings in one Na+ with glucose

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15
Q

What does SGLT1 transporter rely on?

A

Na+/K+ ATPase pump on the basolateral side

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16
Q

What transporter is present for fructose absorption?

A

GLUT5 transporter on the apical membrane

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17
Q

What transporter is responsible for glucose/ fructose absorption into the intracellular fluid?

A

GLUT2 (on basolateral side) via facilitated diffusion

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18
Q

What is glucose-galactose malabsorption syndrome? What would this lead to?

A

Genetic condition where SLGT1 is mutated, so there is no absorption of glucose or galactose. Leads to severe and potentially fatal diarrhoea in infants

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19
Q

Which transporter absorbs 50% of amino acids as di and tri peptides?

A

PepT1 transporter, uses a proton gradient (i.e. absorbed peptides with H+)

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20
Q

How does pancreatic lipase digest fat?

A

Breaks down triglycerol into monoacylglycerole and 2 free fatty acids (reversible)

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21
Q

Fat digestion is dependent on bile salts - what is the role of bile salts?

A
  • Emulsification of large fat droplets, i.e. breaks them down to increase SA for action of lipase
  • Formation of mixed micelles, which stabilise products of triglyceride hydrolysis while they are ‘translocated’ to the apical memrbane
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22
Q

What is the consequence of not having bile? i.e. in liver disease

A

Steatorrhea (fatty diarrhoea)

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23
Q

What is the pKa of free FA? What does this mean?

A

pKa = 4.9
This means that at pH of 4.9, 50% of fatty acids will be in the dissociated form and simple diffusion is possible.

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24
Q

How does pH influence the state of FA?

A
  • Decreasing pH <4.9 = more dissociative form
  • Increasing pH > 4.9 = less dissociated form
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25
Q

What are the proposed transporters for free fatty acids?

A

FAT and CD36

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26
Q

What happens after monoacyglycerol and FA are absorbed?

A

Triglyceride re-synthesis in the ER, packaged into chylomicrons. They leave the enterocyte via chylomicrons, and are transported in the lymphatic system (lacteals) to the liver (enter the blood via thoracic duct)

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27
Q

Where is cholesterol absorbed and what is it dependent on?

A

Duodenum
Dependent on NPC1L1 protein - which allows for receptor-mediated endocytosis

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28
Q

What drug targets the NPC1L1 protein?

A

Ezetimibe - inhibits endocytosis to reduce plasma cholesterol

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29
Q

Give some examples of short chain fatty acids

A

Butyrate, propionate, acetate

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30
Q

What transporter is responsible for absorption of short-chain fatty acids in the colon?

A

SMCT1

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31
Q

What is osmotic load and what can it lead to?

A

Incomplete digestion and absorption of food, leads to increased fluid in the colon and thus in the faeces (= diarrhoea)

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32
Q

Give some examples of how lack of enzymes/ transporters can lead to osmotic load, and how this alters stool consistency

A
  • Congenital causes: watery = glucose-galactose malabsorption (SGLT1) or lactase deficiency
  • Disease of pancreas and biliary systems: leads to steatorrhoea, i.e. pancreatitis, CF, hepatitis, gall stones
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33
Q

Give examples of what can damage mucosal cells, leading to osmotic load

A
  • Autoimmune/ immune diseases: coealic disease, Crohns
  • Infections: bacteria, i.e. shigella (destroys intestinal wall)
  • Salmonella: inflammation of intestinal wall
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34
Q

What is recommended to treat individuals suffering from cholera and why?

A

Oral rehydration therapy: the toxins inhibit Na+ absorption but not the SGLT1, therefore give individuals water with salt and glucose - enhances water transport into the body with the gluocse

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35
Q

How are fat-soluble vitamins absorbed?

A

Vitamins A, D, E and K
- At very low concentrations they require facilitated diffusion and/or endocytosis
- Required optimal fat digestion

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36
Q

How are water-soluble vitamins absorbed?

A

Vitamins B and C
- Specific transporters; facilitated diffusion and secondary active transporter
- Exception = B12 is via endocytosis (uses intrinsic factor)

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37
Q

Describe the transcellular route of calcium absorption

A

1: calcium enters via TRPV6 channel, down its electrochemical gradient
2: Ca2+ is sequestered to calbindin to prevent damage to the cell and enable movement to the basolaterla membrane
3: Calcium is removed by active transport via Ca2+ ATPase (PMCA) - expends Ca2+ out of the cell

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38
Q

Describe the parcellular route of calcium absorption

A

Crosses the epithelium down the concentration gradient

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39
Q

What does absorption of Ca2+ depend on and why?

A

Vitamin D (1,25-dihydroxy-vitamin-D) = transcription of mRNA which encodes for PMCA, calbindin and TRPV6

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40
Q

What route is iron absorbed down and where does this occur in the GI tract?

A

In the duodenum via transceullar routes

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41
Q

How can iron enter over the apical membrane?

A
  • Via DMT: transports ferrous form (reduced) Fe2+ across with the transport of H+
  • Via Heme
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42
Q

How does heme transport iron into the cell?

A
  • Heme = protein bound to Fe2+
  • Inside the cell it is oxidised to release Fe2+ = ferric irons
  • Then reduced again = ferrous irons
  • Ferrous iron binds to mobilferrin as it is toxic, and moves it to the basolateral membrane
  • Iron leaves the cell via FP1
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43
Q

What happens after ferrous iron leaves the cell via FP1?

A

Ferrous irons are re-oxidised to ferric irons (Fe3+), and bind to transferrin

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44
Q

What catalyses the oxidation of iron?

A

hephaestin

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45
Q

After oxidation of heme releases Fe2+, what does the remainder of the heme proteins produce?

A

biliverdin, a precursor of bilirubin
(excreted in bile)

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46
Q

What regulates iron absorption? How?

A

Hepcidin, produced by the liver when you have enough iron. It is secreted into the blood and results in internalisation of FP1 = inhibit step of iron exiting the cell. this means iron is stored in enterocytes, bound to mobilferin (then lost by faeces)

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47
Q

How is gastric pain vs pancreatic pain differentiated?

A

Pancreatic pain radiates to the back, gastric pain tends to stay localised to the epigastrium

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48
Q

What is cachexia?

A

Inflammatory condition that is disease related. It can be linked to malnutrition and be chronic or acute.

49
Q

What can cachexia lead to?

A
  • Increased protein catabolism
  • Decreased absorption
  • Increased energy expenditure
  • Inflammation, leading to lower FM and FFM via the above
50
Q

What is sarcopenia?

A

Geriatric condition witht he natural aging process, where have reduced protein synthesis. this leads to reduced FFM (gradually) and reduced muscle function.

51
Q

How is sarcopenia differentiated from cachexia?

A

Cachexia: rapid and acute loss of skeletal muscle
Non-cachexia related sarcopenia = gradual and progressive loss of muscle mass

52
Q

How is cachexia graded by % weight loss?

A

In the last 12 months:
- Mild = if weight loss > 5%
- Moderate = if > 10%
- Severe = if > 15%

53
Q

Compare nutritional screening and assessment

A

Screening: general, simple, quick, often performed at first contact with a patient.

Assessment: specific evaluation, more time consuming, completed when serious problems are identified.

54
Q

What is patient-generated subjective global assessment (PG-SGA) used for?

A

Cancer patients - modified version of SGA. Subjective, short form to be completed by patients and then the full form by HCP (no anthropometric measurements)

55
Q

Which nutritional screening tool utilises anthropometric measurements?

A

Malnutrition universal screening tool (MUST)

56
Q

What does a deficiency in the following lead to?
- C/K vitamins
- Essential FA
- Fe/ B vitamins

A

C/K = bruising
Essential FA = dry skin
Fe/B = mouth ulcers, atrophic tongue

57
Q

What does anthropometry measure? What is a benefit/ disadvantage?

A

Weight and height (BMI), waist and hip circumference, mid-arm muscle circumference (MAMC)
- Benefit = cheap
- disadvantage= doesn’t differentiate muscle and fat

58
Q

How might body composition be differed in someone with sarcopenic obesity?

A
  • Significant muscle wastage
  • High subcutaneous fat deposition
59
Q

What measurements of nutritional assessment should be used for cancer patients?

A

Body composition, because anthropometry doesn’t show fat/ muscle tissue and therefore can inaccurately give chemotherapy doses

60
Q

How can body composition be measured?

A
  • Bio impedance analyser
  • Dual X-ray absorptiometry (DEXA)
  • CT
  • ADP
61
Q

What is acute pancreatitis?

A

Sudden onset, life-threatening inflammation of the pancreas. Usually reversible but leads to autodigestion via intra-pancreatic activation of trypsin.

62
Q

What are signs/symptoms of acute pancreatitis?

A
  • Severe abdominal pain in epigastrium, may radiate to back
  • Nausea and vomiting
  • Haemorrhaging
  • Respiratory distress
  • Fever
  • Shock: hypotension, tachycardia
63
Q

What is Cullens sign? What might it indicate?

A

Superficial oedema with bruising around the peri-umbilical region. Can indicate haemorrhagic pancreatitis

64
Q

What is Grey turners? What might it indicate?

A

Discoloration of the flanks. Represents retroperitoneal haemorrhage

65
Q

What can cause acute pancreatitis? State which 2 causes are the most common

A

‘I GET SMASHED’
I: Idiopathic
G: Gall stones - common
E: Ethanol - common
T: Trauma
S: Steroids
M: Mumps
A: Autoimmune
S: Scorpion sting
H: Hypertriglyerides
E: ERCP
D: Drugs

66
Q

What investigations may be done to check for acute pancreatitis?

A
  • Clinical exmination: severe abdominal pain, blood test for amylase and lipase
  • Chest x-ray to exclude perforation
  • CT scan: assess for pancreatic necrosis, abscess or fluid collection
67
Q

Why would an ultrasound not be used to investigate acute pancreatitis?

A

The transverse colon overlies the pancreas so air can interfere with the image

68
Q

Name the 2 scales that can assess the severity of acute pancreatitis and how they work?

A

Glasgow imri criteria: checks markers, if more than 3 are present in 48h then indicates a severe attack
Atlanta classification: depends on organ dysfunction/ failure (mild = none, moderate = transient failure or dysfunction, severe= persistent)

69
Q

What is a good marker for acute pancreatitis and why?

A

Albumin; as tissue permeability increases then you leak more albumin

70
Q

What are common complications of acute pancreatitis?

A

Acute fluid collection:
- Walled off pancreatic necrosis: dying/ non-viable pancreatic tissue, involves an infection
- Pseudocysts: organised fluid collections lined by granulation tissue (no infection)

71
Q

What is chronic pancreatitis?

A

Chronic, continuous inflammation, that leads to fibrotic changes, loss of tissue, and acinar to ductal metaplasia. There is loss of functional units and impaired pancreatic functioning

72
Q

What is the pathogenesis of acinar fibrosis?

A

1: Increased acinar protein (and zymogen enzyme) secretion, decreased sodium bicarbonate and fluids
2: increased viscosity pancreatic duct plugging
3: zymogens fuse with lysosomes - activate trypsinogen -> trypsin = digests the pancreas
4: Acinar atrophy and fibrosis

73
Q

What are the 3 forms of chronic pancreatitis?

A
  • Chronic calcifying pancreatitis
  • Chronic obstructive pancreatitis
  • Chronic autoimmune pancreatitis
74
Q

What is chronic calcifying pancreatitis? What is it caused by?

A

Early stages characterised by acute pancreatitis, development of stones and atrophy.
Causes = alcohol, smoking, idiopathic, genetic

75
Q

What is chronic obstructive pancreatitis?

A

Results from primary injury to the duct of partial- complete obstruction. Often asymptomatic, but partial obstruction can lead to bouts of acute pancreatitis

76
Q

What are the 2 types of chronic autoimmune pancreatits?

A
  • Type 1: IgG4-related disease. Has increased IgG4 and multiorgan involvement
  • Type 2: idiopathic, neutrophils damage pancreatic ducts (no other organ involvement)
77
Q

What are some of the causes of chronic pancreatitis?

A
  • Alcohol (60-70%)
  • Idiopathic (20-30%)
  • Autoimmune, i.e. IgG4
  • Hyperlipiadaemia
  • Genetic
78
Q

What 3 genes can cause chronic pancreatitis?

A
  • CFTR = cystic fibrosis
  • SPINK1= trypsin inhibitor in pancreatic acinar cells, progression of AP to CP
  • PRSS1 = codes for trypsinogen (premature activation)
79
Q

What are some important symptoms of chronic pancreatitis?

A
  • Pain = radiating from epigastric to back
  • Diarrhoea/ Steatorrhea
  • Weight loss
  • Jaundice if bile duct is obstructed
  • Diabetes type 3 - later in the disease due to loss of B cells
80
Q

What investigations are done for chronic pancreatitis?

A
  • Faecal elastase 1 = indirect mreasure, quantifies elastase in your stool
  • CT of abdomen (if not improving after 2/3 days), can also do it after injecting secretin to assess volume of digestive juice produced
  • Endoscopic ultrasound
81
Q

How is chronic pancreatitis treated/ managed?

A

Mainly supportive - treat underlying cause
1: lifestyle- stop smoking, reduce alcohol
2: treat malabsoprtion; replace pancreatic enzymes with pancreatin/ Creon (combines protease, lipase and amylase) - take before and during meals. May be given with PPI
3: treat complications, i.e. diabetes, stones
4: pain control - NSAIDs, opiates, neuropathic (TCAs, SSRIs)

82
Q

What is type 3c diabetes?

A

‘Pancreaticogenic diabetes’: 5-10% of all diabetes, difficult to manage. Usually has low insulin requirements

83
Q

What are some complications of chronic pancreatitis?

A
  • Pseudocysts (can test using fine needle aspiration)
  • Variceal bleeding= as splenic vein runs across the pancreas
  • Obstruction of bile duct/ duodenum
  • Acute respiratory distress syndrome
  • Haemorrhage -> Cullens and grey turner signs
84
Q

When would you screen a patient with chronic pancreatitis for adenocarcinoma?

A

If they had these symptoms present:
- Increased pain
- Weight loss
- Obstructive jaundice

85
Q

How does alcohol lead to feelings of pleasure?

A

Binds to opiate receptor, leads to release of endorphins which bind to dopaminergic receptors to increase dopamine and serotonin (mesolimbic pathway)

86
Q

What are 3 main complications of alcohol disorder?

A

1- liver disease: portal hypertension = liver cirrhosis = blood cant pass though, can lead to ascites
2: Wernicke’s encephalopathy: thiamine B12 deficiency, leads to ataxia, confusion and ophthlamoplegia
3: Korsakoff’s psychosis: confabulation (waffling about nothing), ataxia, short-term memory loss

87
Q

What are delirium tremens?

A

Delirium with hallucinations and autonomic disturbances during alcohol withdrawal. Leads to anxiety attacks, increasing confusion, poor sleep, profuse sweating and depression.

88
Q

If someone cannot adhere to an alcohol detox programme why would you recommend them to carry on drinking?

A

Due to risk of severe withdrawal seizures (10% mortality), peak incidence 1-2d after a drink

89
Q

What peripheral symptoms may someone suffer from with an alcohol disorder?

A

Polyneuropathy - affects sensation/ tingling
Myopathy- proximal muscle wasting

90
Q

What is the ICD-10 definition of alcohol dependence?

A

A disorder of regulation of alcohol use, it involves:
- Repeated or continuous use of alcohol
- Strong internal drive to use alcohol
- Present for 12 months, or 1 month if continuous

91
Q

What are some key symptoms of alcohol dependence?

A
  • Internal drive, compulsion, desire, urge or craving to use alcohol
  • Impaired control
  • Prioritisation of alcohol over other activities
  • Persistent use despite harms
  • Tolerance and withdrawal symptoms = neuroadaptation
92
Q

What is the Kindling phenomonen?

A

Repeated episodes of withdrawal followed by excessive drinking causes seizures which can lead to death

93
Q

What is alcohol hallucinosis? When do they occur?

A

Hallucinations (usually visual) without other impairment of consciousness, usually within 12-24 hours of withdrawal.

94
Q

What is the pathophysiology of alcohol withdrawal?

A

1: glutamate becomes overactive (as its normally inhibited by alc), and GABA is underactive (stimualted by alc)
2: GABA-A receptors downregulated and NMDA receptors upregulated
3: brain overexcitability = delirium, seizures, hallucination, headache, confusion, anxiety
4: Increased cortisol from HPA axis

95
Q

What drug can be given to prevent Wernicke Encephalopathy during severe alcohol withdrawals?

A

IV thiamine (100mg) [i.e. give if deficient in B vitamins]

96
Q

What drugs may be given during alcohol withdrawals to treat agitation and prevent seizures?

A

Benzodiazepines, i.e. diazepam or chlordiazepoxide

Or give phenobarbital (or both)

97
Q

What medication may be given to help someone overcome their addiction to alcohol? Give its MOA

A

Disulfiram: inhibits alcohol dehydrogenase, gives a horrible reaction = sweating, nausea, palpitations = in attempt to prevent them drinking again

98
Q

What medication may be given to help prevent relapse of alcohol disorder? Give its MOA

A

Acamprostate: inhibits voltage-gated calcium channels to decrease excitatory overdrive to help anxiety and sleep

99
Q

During alcohol withdrawal, when do delirium tremens and seizures reach their peak incidence?

A

Seizures: 1-2d after last drink

DT’s: 5d after last drink

(key to remember seizures occur early but confusion occurs late)

100
Q

What are the 3 main patterns of alcohol dependence?

A

1: binge intoxication
2: withdrawal negative affect
3: preoccupation anticipation
(in between is neuroadaptation)

101
Q

What is the gold-standard screening test for alcohol disorder? What score requires action?

A

AUDIT (alcohol use disorders identificiation test) screening: can do the FAST version, then if positive complete the full AUDIT (10 Qs) .
Score >20 requires action
16-19= harmful drinking
8-15= hazardous

102
Q

What is asked within the CAGE questionnaire?

A

C: Have you every felt you needed to cut down drinking?
A: Have people annoyed you by criticising your drinking?
G: Have you ever felt guilty about drinking?
E: Have you ever felt you needed a drink in the morning (eye-opener) to steady nerves or to get rid of a hangover?

103
Q

What is the brain disease model of addiction?

A

Views addiction as a brain disease, may be useful to reduce stigma and increase treatment seeking behaviour

104
Q

What is the theory of allostasis?

A

Reduced reward feelings from alcohol and increased stress over time = attempt to return to baseline of high reward/ low stress = drink more to return to the same level

105
Q

Compare classical and operant conditioning theories of addiction

A

Classical: environment around the drug (bar/ pub) is associated with taking the drug/ alcohol, so now the environment stimulates cravings for alcohol
Operant: Positive and negative feedback loops - euphoria of drinking alcohol makes you drink more, and the withdrawal symptoms make you want to drink more too

106
Q

Where are the highest rates of alcohol consumption in England?

A

North West

107
Q

What interventions were recommended by Public Health England review to reduce alcohol intake?

A
  • Increasing price (taxation) = most-effective
  • Complete marketing ban; prevents childhood exposure to marketing
  • Lower legal alcohol limit for young drivers
  • Brief advice
  • Reduce the hours in which alcohol is available for sale
108
Q

What is the HARK questionnaire? What is a positive score?

A

Humiliation, Afraid, Rape, Kick: 4 questions to identify women experiencing partner violence int he past year.

One point given for each question (i.e. within the last year have you been humiliated or emotionally abused in other ways by your partner/ex partner). A score 1+ is positive for intimate partner violence (IPV)

109
Q

Apply the 5 areas model to someone living with an abusive partner

A
  • Situation: living with abusive partner
  • Thoughts: “i need a drink to cope”, “im scared of him”
  • Physical sensations: shaking, racing heart, increased breathing
  • Behaviours: drinking every weekend
  • Feelings: stress, worry, guilt
110
Q

What is potomania?

A

Electrolyte disturbance from excessive drinking of alcohol without a proper diet

111
Q

What is dipsomania?

A

Uncontrollable craving for alcohol

112
Q

What is the UK guideline for safe drinking?

A

14 units/ week, spread use over 3 days if drinking 14 units

113
Q

What is binge drinking defined as?

A

> 8 units in men or >6 units in women

114
Q

How can alcohol affect the oesophagus?

A

Can lead to squamous carcinoma of the oesophagus. Oesophageal varices are associated with chronic liver disease

115
Q

What is the main cause of mortality from alcohol dependence? What increases risk of this?

A

Alcohol related liver disease, i.e. alcohol hepatitis or cirrhosis. Higher risk if:
- >9 units/day
- Women
- Obesity

116
Q

What does the duodenum mainly absorb?

A

iron

117
Q

What signs might patients present with if they are suffering from domestic abuse?

A
  • Physical injuries
  • Bedwetting, sleeping problems
  • frequently attending or missing appointments
  • Appearing fearful
  • Frequent use of analgesia or sleeping pills
118
Q

What is the role of enterokinase?

A

Activates trypsinogen to trypsin for protein digestion

PBL Y2 S4 (9 decks)

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