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Consolidation by CBL > CBL 1 (W1-2) Liver > Flashcards

CBL 1 (W1-2) Liver Flashcards

1
Q

What are the typical signs and symptoms of a patient with Cholera?

A

-Severe Diarrhoea
-Dehydration
-Vomiting
-Abdominal pain

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2
Q

What are the typical signs and symptoms of a patient with Tetanus?

A

-Muscle Spasm
-Fever
-Lockjaw
-Dysphagia

Way to remember:
TetANUS
My Farts Linger Daily

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3
Q

What are the typical signs and symptoms of a patient with Typhoid?

A

-Fever
-Headache
-Abdominal pain
-Constipation
-Rash

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4
Q

What are the typical signs and symptoms of a patient with Hepatitis?

A

-Abdominal pain
-loss of appetite
-fatigue
-dark urine
-pale stool
-jaundice

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5
Q

What are the typical signs and symptoms of a patient with TB ?

A

-Chest pain
-Weight loss
-Loss of appetite
-Night sweats
-Haemoptysis

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6
Q

What is the incubation period/onset of Hepatitis?

A

1.5-6months

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7
Q

What is the incubation period for Salmonella?

A

6hrs-6months

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8
Q

What causes the classical symptoms of an acute infection? i.e Fever, Malaise, Aches, Pains and Nausea?

A

The body produces cytokines such as Interferon which causes the global effects.

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9
Q

What are the prehepatic causes of jaundice?

A

=Excessive RBC breakdown
-Thalassaemia, Haemolytic anaemia, spherocytosis, sickle cell anaemia

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10
Q

What are the intrahepatic causes of jaundice?

A

=Dysfunction of hepatic cells / less hepatocytes and therefore reduced ability to conjugate bilirubin
-Viral Hepatitis
-Alcoholic Cirrhosis
-Drug induced jaundice
-Alcoholic hepatitis
-Autoimmune liver disorders

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11
Q

What are the Extrahepatic causes of jaundice?

A

=Obstruction of biliary drainage which causes hyperbilirubinemia
-Gallstones
-Cancer
-Pancreatitis

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12
Q

What is Kernicterus?

A

When a baby with Jaundice gets seizures and muscle spasms due to brain damage from the bilirubin crossing the BBB.

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13
Q

What is unconjugated bilirubin?

A

Bilirubin is bound to albumin in the blood, is therefore insoluble in water and cannot be excreted.

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14
Q

What is conjugated bilirubin?

A

Not bound to Albumin, therefore water soluble and can be excreted from body.

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15
Q

Explain bilirubin formation.

A

From the breakdown of RBCs.
-Macrophages (Reticuloendothelial cells) break haemoglobin down into globin and haem (which is reduced to iron and Biliverdin via enzyme Haem Oxygenase). Iron is recycled and Biliverdin is reduced to unconjugated bilirubin

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16
Q

What is Gilbert’s syndrome?

A

It is a hereditary condition which causes Hyperbilruinaemia due to a Glucuronyl Transferase Definciency and therefore Bilirubin conjugation is slower and therefore less is excreted.

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17
Q

How are patients with Gilbert’s Syndrome affected?

A

Asymptomatic with normal bilirubin levels however they can become easily and quickly jaundiced when physically stressed.

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18
Q

What gene is affected in Gilbert’s syndrome?

A

UGT1A1

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19
Q

How is neonatal jaundice treated?

A

Phototherapy

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20
Q

How does carcinoma of the pancreas cause jaundice?

A

Enlargement of the pancreas causes the common bile duct to compress leading to jaundice.

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21
Q

How is carcinoma of the head of the pancreas treated?

A

Pancreatoduodenectomy by Whipple resection (removal of the head)

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22
Q

How does gallstones (aka Cholethiasis) cause jaundice?

A

Causes obstruction of the biliary system resulting in biliary colic and jaundice.

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23
Q

How does Malaria cause jaundice?

A

P.falciparum parasite causes intravascular haemolysis which causes and increase in Bilirubin and therefore Jaundice.

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24
Q

How are gallstones obstructing bile ducts treated?

A

Inserting a stent using ERCP or Laparoscopic Cholecystectomy

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25
Q

How is Malaria treated?

A

Schizonticides
=type of chemotherapy that kills the parasite in the blood

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26
Q

What is the meaning of febrile?

A

Fever

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27
Q

What is the meaning of Icteric?

A

Jaundice

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28
Q

What are the 3 main causes of Chronic Liver Disease?

A

-Hepatitis
-Haemochromatosis
-Non Alcoholic Fatty Liver Disease

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29
Q

What are the causes Abdominal Distension?

A

6Fs- Fat, Fluid, Flatus (gas), Faeces, Fetus, Fuminant mass (a smelly mass)

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30
Q

What are Caput Medusae?

A

Engorged paraumbilical veins

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31
Q

What is associated with Caput Medusae?

A

Portal Hypertension caused by Liver Cirrhosis

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32
Q

What are the causes of Striae (stretch marks)?

A

Ascites, intrabdominal malignancy, cushing’s syndrome, obesity and pregnancy

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33
Q

What is Cullen’s sign?

A

Bruising of tissue surrounding the umbilicus

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34
Q

What is Cullen’s sign associated with?

A

Haemorrhagic Pancreatitis (late sign)

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35
Q

What is Grey-Turner’s sign?

A

Bruising in the flanks

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36
Q

What is Grey-Turner’s sign associated with?

A

Haemorrhagic Pancreatitis

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37
Q

What does a high ALP and normal GGT mean?

A

ALP and GGT raised indicate and obstruction problem with the liver.
So if GGT isn’t raised, raised ALP will indicate an issue with Bones (e.g Paget’s Disease)

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38
Q

What does a high ALP AND GGT indicate?

A

ALP and GGT raised indicate and obstruction problem with the liver.

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39
Q

Other than obstruction of the liver, what else can a raised GGT indicate?

A

Too much alcohol consumption or Obesity

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40
Q

What does a raised AST and a normal ALT indicate?

A

AST AND ALT raised would indicate damage to the hepatocytes (liver). But if only AST is raised, that would instead point to muscle damage.

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41
Q

What does a raised AST and ALT indicate?

A

Damaged liver perhaps due to drugs or alcohol. Will want to check for inflammation and fibrosis (i.e Cirrhosis).

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42
Q

What does an elevated T.Bilirubin indicate?

A

Bile duct / Liver issues, or Haemolytic Anaemia

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43
Q

What is Mastication?

A

The voluntary activity involving skeletal muscle to aid the chewing reflex.

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44
Q

What are the functions of mastication?

A

-Prevents airway obstruction
-Lubrication and digestion
-Increase the surface area exposed to secretions

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45
Q

What is the function of amylase?

A

To breakdown starch

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46
Q

What is the function of mucous in the mouth?

A

To lubricate food

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47
Q

What are the 3 stages of swallowing?

A

1.Voluntary (oral) stage = Bolus squeezed into pharynx by tongue

2.Pharyngeal stage = food goes into oesophagus and epiglottis protects it going into the air tract

3.Oesophageal stage = Transport of food from pharynx into stomach via peristaltic contractions

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48
Q

What is the function of the epiglottis during swallowing?

A

It swings during the pharyngeal stage to protect the airway tract.

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49
Q

Where is the swallowing centre located?

A

Medulla Oblongata

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50
Q

What is the purpose of the soft palate during the pharyngeal stage of swallowing?

A

To prevent nasal reflux

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51
Q

During swallowing, the opening of the oesophagus enlarges. How does this happen?

A

The larynx is squeezed shut and pushed upwards which makes the opening bigger.

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52
Q

Describe the musculature of the oesophagus (i.e the type of muscles present).

A

-Upper 1/3 = Striated muscle

-Lower 2/3 = Smooth muscle

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53
Q

What innervates the muscles of the oesophagus?

A

Glossopharyngeal and Vagus nerves

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54
Q

What is primary peristalsis?

A

When the food bolus is present in the oesophagus

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55
Q

What is secondary peristalsis?

A

When the oesophagus distends and the bolus moves down towards the oesophageal sphincter and stomach

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56
Q

What is the Vagovagal reflex?

A

Relaxation of the fundus and body of the stomach to take up to 1.5L of contents

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57
Q

During the emptying of the stomach, what muscle is involved?

A

Circular longitudinal oblique muscle in the Antrum of the stomach to produce intense peristaltic contraction to constrict the Pyloric Sphincter

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58
Q

Describe the electrical activity of the GI smooth muscle.

A

Partial depolarisation sweeps along the digestive tract across long distances:
1.Slow waves stimulate the spike potentials
2.Spike potentials happen at -40mV

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59
Q

What causes the GI smooth muscle to stretch?

A

Parasympathetic innervation via Acetylcholine

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60
Q

What reduces GI smooth muscle contraction?

A

Sympathetic innervation via Noepinephrine.

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61
Q

What is the pyloric pump and what causes it?

A

It is the backwards force caused by the spike potential which causes a tightening ring around the pylorus. This regulates the rate of gastric emptying.

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62
Q

How does the contents of the interstitial lumen affect gastric emptying?

A

Depending on what is present in the intestine (from gastric emptying), chemoreceptors feed this back to Intramural intrinsic plexuses that feed it back to the CNS to organise sympathetic and parasympathetic activity.

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63
Q

If there are amino acids present in the intestine what will the stomach produce?

A

Gastrin

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64
Q

If there are fats present in the intestine what will the stomach produce?

A

Cholecystokinin to get the gallbladder and pancreas to contract.

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65
Q

If there is acid present in the intestine what will the stomach produce?

A

Secretin

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66
Q

What metabolic effects happen as a result of vomiting?

A

Loss of NaCl, H20, H+
=Metabolic alkalosis

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67
Q

What % does the duodenum, jejunum and ileum make up of the small intestine?

A

Duodenum- first 5%

Jejunum - 40%

Ileum - 55%

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68
Q

What is Mesentary ?

A

Mesentary attaches to the abdominal wall with lymphatics (draining) and vessels.

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69
Q

What is the meaning of Migratory Motility Complex of the Small intestine?

A

The mass clearance of the small intestine. Waves of electrical activity burst to limit the overgrowth of harmful bacteria.

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70
Q

What causes the bursts of electrical activity in the Migratory Motility Complex?

A

When in the fasted state, the hormone Motilin is released which increases vagal impulses and therefore the movement and emptying of the SI.

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71
Q

What prevents fecal backflow into the small intestine?

A

The Ileocecal valve

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72
Q

What opens the ileocecal valve to empty the contents of the small intestine?

A

Gastroileal reflex that is regulated by pressure and chemical irritation

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73
Q

What are the functions of the colon?

A

-Absorption of water and electrolytes

-Storage of fecal matter

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74
Q

How are short chained fatty acids produced?

A

After 8-15hrs hours transit time of the chyme, cholonic bacteria arises which synthesises it.

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75
Q

What are mass movements and how often do they occur?

A

Propulsive movement after eating. Happens 1-3 times per day for about 30 secs over a periods of 30minutes. This sustained contraction leads to defecation.

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76
Q

What is the Gastrocolic reflex?

A

Increase of mass movements that is mediated by the autonomic nervous system releasing gastrin.

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77
Q

What happens in the defecation reflex?

A

-There is an increase of afferent signals in the myenteric plexus that causes peristalsis in the colon and sphincter relaxation.
-The parasympathetic activation fortifies the reflex involving the sacral segments of the spinal cord .

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78
Q

How would you treat a patient with Diarrhoea?

A

-Cessation of eating
-IV rehydration with H2O, NaCl and Sucrose to decrease the gut motility

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79
Q

What do carbohydrates breakdown to?

A

Carbs–>Glucose–>Pyruvate–>Acetyl CoA –> Goes through the TCA cycle to produce ATP

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80
Q

How is glucose transported across cell membranes?

A

Facilitated diffusion
NOTE: that it is therefore limited by the availability of transporters.

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81
Q

Where are GLUT1 transporters located?

A

Most tissues (e.g brain, RBCs and Cornea)

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82
Q

Where are GLUT 2 transporters located?

A

Liver, kidney, pancreatic B cells

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83
Q

Where are GLUT3 transporters located?

A

CNS and other tissues

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84
Q

What do GLUT1 transporters do?

A

Basal glucose uptake

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85
Q

What do GLUT2 transporters do?

A

Removes excess glucose from blood in the liver and regulates insulin release in the pancreas.
Note: GLUT2 has a lower affinity for glucose

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86
Q

What do GLUT3 transporters do?

A

Basal glucose uptake

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87
Q

Where are GLUT 4 transporters located?

A

Skeletal muscle and adipose tissue

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88
Q

What do GLUT4 transporters do?

A

They increase during exercise due to insulin.

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89
Q

Where is Insulin produced?

A

Pancreatic B-cells in the Islets of Langerhans

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90
Q

How is insulin degraded?

A

In the Liver by Insulinase.

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91
Q

How does Insulin affect adipose tissues?

A

Increases glucose uptake and Lipogenesis and decreases Lipolysis.

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92
Q

How does Insulin affect the Liver?

A

Increases Glucose synthesis and Lipogenesis and decreases Gluconeogenesis.

IN the Liver, Glucose INcreases with Insulin
(opp of effects around the body)

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93
Q

How does Insulin affect the Striated muscle?

A

Increases Glucose uptake, glycogen synthesis and protein synthesis.

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94
Q

Under fasting conditions, what provides energy?

A

Fatty acids

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95
Q

How does insulin affect GLUT4 transporters?

A

Increases GLUT4 levels and glucose uptake by 15-20 fold.

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96
Q

Why is the brain so highly dependant on Glucose?

A

It is it’s primary energy source. Insulin has minimal effect on glucose. GLUT1 transporters in the brain have the highest affinity for glucose and therefore readily take it up.

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97
Q

What is Hypoglycaemia?

A

Low glucose causes nervous system instability leading to fainting, convulsions and a coma if prolonged (since the brain is highly dependant on glucose).

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98
Q

What are the effects of Glucagon in the liver?

A

Glucagon receptor signalling increases cAMP and PKA to stimulate glycogen phosphorylase to break down glycogen into glucose (glycogenolysis).

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99
Q

How does exercise affect glucagon secreation?

A

Increases it

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100
Q

How does Adrenaline/Noradrenaline affect glucose metabolism?

A

=a-adrenergic activation –> Increase Glycogenolysis –>Increases Glucose

=B-adrenergic activation –>Increase Lipolysis

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101
Q

How does Cortisol and Growth hormone affect glucose metabolism?

A

-Stimulates hepatic gluconeogenesis
-Decreases tissue glucose uptake
-Increases Lipolysis

Note: Stress hormones are protective for hypoglycemia.

Way to remember:

When growing you are preparing the body for long term regulation of your glucose hence the liver stimulation of Glucagon to increase your glucose when needed. Skinning kids, so lipolysis and decrease glucose uptake.

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102
Q

Where is glucose reabsorbed in the kidney?

A

Proximal tubule

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103
Q

What does the SGLT1 and SGLT2 cotransporter do?

A

Transports Na+ and Glucose together into the intracellular space (from the proximal tubule) for the GLUT2 transporter to transport it into the cell (of the blood). Na+ is transported further via the Na/K ATPase pump.

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104
Q

How does blood glucose affect the osmorality?

A

Increases it (causing water loss) and as it is increased in the renal tubules, less is absorbed.

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105
Q

What is Glucotoxicity?

A

Glucose in high levels causes the alteration (glycation) of proteins (HbA1c) and increases reactive oxygen species causing aberrant cellular messaging, chronic inflammation, endothelial dysfunction and B-cell (pancreas) dysfunction

=TISSUE DAMAGE

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106
Q

Describe the switch to fat metabolism when Insulin is not present?

A

Insulin inhibits Lipase…so without insulin means Lipase is NOT inhibited.

Lipase is the enzyme that allows triglycerides –> Free Fatty acids —> (via B-oxidation) =KETONES

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107
Q

How is Diabetic Ketoacidosis caused?

A

-Lack of metabolism
->Ketone production
–>Decreases pH and increases H+
=METABOLIC ACIDOSIS
—>Hyperkalaemia

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108
Q

What tests are used for diagnosing diabetes?

A

-Urinary glucose
-Fasting blood glucose
-Fasting plasma insulin
-Glucose tolerance test

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109
Q

What Urinary glucose would you expect from a diabetic patient and why.

A

> 10mmol/L as the renal capacity for reabsorption is exceeded

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110
Q

What are the normal ranges for fasting blood glucose and fasting plasma insulin?

A

Glucose: 3.4-6.2
Insulin: 10mU/mL

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111
Q

What result would you expect from a Glucose Tolerance test from a Diabetic patient?

A

Delayed decrease of blood glucose after an oral bolus.

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112
Q

How quickly are Amino acids absorbed compared with Glucose?

A

SLOW (glucose in comparison is VERY fast)

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113
Q

What is the Deamination of Amino Acids?

A

The breakdown of AAs that gives rise to Glucose, Fatty Acids and Ketone bodies; or breaks into Ammonia and goes through the urea cycle to give urea.

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114
Q

Unlike glucose and fatty acids, amino acids cannot be stored. What happens instead?

A

Free Amino acids quickly combine to form peptides and intracellular proteins.

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115
Q

How does Growth hormone and insulin affect protein synthesis?

A

Increase

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116
Q

How do Glucocorticoids affect protein synthesis?

A

Decrease- as they mobilise amino acids (breakdown proteins)

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117
Q

What does the protein transferrin do?

A

Carries the ferrous iron in the circulation

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118
Q

What plasma protein is the most abundant?

A

Albumin

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119
Q

How does Liver disease affect protein synthesis and how does this physically manifest?

A

Decreases protein synthesis causing Oedema

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120
Q

What are the temporary use of energy stores in absence of glucose (in order of usage).

A

1.Fat
2.Protein

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121
Q

What does Cachexia mean?

A

Loss of body mass that cannot be reversed nutritionally e.g Cancer, Aids, Coeliac disease, COPD, Congestive heart failure, TB

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122
Q

What does a Hypermetabolic state mean?

A

Elevated levels of cytokines which promote protein breakdown e.g Burns, Trauma, Sepsis

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123
Q

What does a positive nitrogen balance mean and when do you get it?

A

When there is an increased demand for protein e.g growth, pregnancy, recovery from illness/trauma

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124
Q

What does a negative nitrogen balance mean and when do you get it?

A

During starvation/malnutrition= the protein intake is insufficient for normal metabolism

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125
Q

What are the major glands of the mouth?

A

-Submandibular
-Sublingual
-Parotid

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126
Q

Describe the salivary secretions from the Parotid glands.

A

Watery (Serous) = Contains proteins (enzymes e.g Amylase)

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127
Q

Describe the salivary secretions from the Submaxillary glands.

A

Mixed serous and mucous secretion (thicker substance)
-Makes up 70% of secretions in the mouth

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128
Q

Describe the salivary secretions from the Sublingual glands.

A

Mucous (mainly)

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129
Q

What is the composition of saliva and what are their functions?

A

99% is water + complex mixture:
-Mucous
-Iron
-Growth factors
-Amylase (starch breakdown)
-Lysozyme (anti-bacterial)
-Bicarbonate (pH buffer)
-IgA (anti-bacterial)
-Epidermal growth factor (EGF) (Maintain tissue integrity

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130
Q

What are the 3 stages of stimulating gastric secretion?

A

Cephalic, Gastric and Intestinal phases

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131
Q

Describe the Cephalic stage of stimulating gastric secretion.

A

Sign of food/thought –>Cerebral Cortex–>Hypothalamus and Medulla Oblongata–>Vagus Nerve –> Stimulates gastric secretions

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132
Q

Describe the Cephalic stage of stimulating gastric secretion during Depression / Loss of Apetite.

A

Depression –> Cerebral cortex –> Lack parasympathetic stimulus –> Inhibits secretory activity

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133
Q

Describe the stages of Gastric secretion.

A

1.Gastrin secreted by G-cells
2.Mechanosensation upon stomach distension (just eaten)–>Parasympathetic signalling via Acetylcholine –>Secretion

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134
Q

What factors can stimulate gastric secretion?

A

Coffee, Peptides, Increase in pH

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135
Q

What is the Enterogastric reflex?

A

A feedback mechanism to control the rate of chyme emptying from the stomach into the small intestine. Stretching of the duodenal wall results in the inhibition of gastric motility and reduces the emptying of the stomach.

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136
Q

What hormone does the intestines produce to counter the acid from the stomach (HCL)?

A

Secretin

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137
Q

What do the duodenal glands produce and why?

A

Bicarbonate rich mucous for buffering

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138
Q

How long does it take till chyme is emptied from the stomach? (Note what order)

A

2-4 hours
1.Carbohydrates (fastest)
2.Protein
3.Fat (slowest: up to 6hrs)

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139
Q

How does the stomach protect / counter itself against the highly acidic enviroment?

A

-Bicarbonate mucous barrier
-Gastric pits with stem cells replace dead cells
-Stomach is COMPLETELY REPLACED: Every 3-6days

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140
Q

What digestive enzymes does the pancreas secrete?

A

-Bicarb
-Proteases (Typsinogen, Chymotrypsinogen, Elastase, Procarboxypeptidase)
-Pancreatic Lipase
-Nucleases (to degrade nucleic acids)
-Amylase

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141
Q

What does secretin do in the duodenum?

A

Stimulates the ducts to release bicarb pancreatic juice to neutralise the HCl.

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142
Q

What 2 duodenum hormones are secreted from the pancreas?

A

-Secretin
-Cholecystokinin (CCK)

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143
Q

What does CCK do in the duodenum?

A

Stimulates the Acini to secrete enzyme-rich pancreatic juice

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144
Q

What initiates Bile release?

A

CCK (Cholecystokinin)

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145
Q

What does Bile do in digestion?

A

Emulsifies lipids

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146
Q

How is Bile recycled?

A

Via Enterohaptic circulation

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147
Q

Where and when in bile stored?

A

In the Gallbladder between meals

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148
Q

Where are the majority of Carbohydrates and proteins absorbed?

A

Jejunum

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149
Q

Where are bile salts and vitamin B12 absorbed?

A

Terminal ileum

150
Q

How are carbohydrates transported when absorbed in the small intestine?

A

Na+ symporters (e.g SGLUT1) and Na+ pumps (to establish gradient)

151
Q

How are fats transported when absorbed in the small intestine?

A

-Bile salts assemble as Micelles
-Fatty acids reassemble into triglycerides –>Chylomicrons –> Lacteal (lymphatic vessels of the small intestine will now absorb)

152
Q

How are amino acids transported when absorbed in the small intestine?

A

Transporters

153
Q

What are the function of the Gut Microflora?

A

1.Vitamin Synthesis = Biotin, Pantothenic acid, Vitamin K
2.Chemical signalling : e.g Gut-Brain axis, Gut-Liver axis
3.Colonisation resistance and inhibit infections by pathogenic bacteria

154
Q

What is Biotin?

A

-Vitamin (Vit 7) found in eggs, milk and bananas.
-Important part of enzymes that break down fats and carbohydrates
-Important for hair

155
Q

What is Pantothenic acid?

A

-Vitamin (Vit B5)
-Involved in the synthesis of CoA

156
Q

What is Vitamin K?

A

=Blood clotting

157
Q

What cells make up the Oxyntic glands of the stomach and what do they do?

A

-Mucous neck cells = Mucous
-Parietal cells = HCl and Intrinsic factor
-Enterochromaffin like cells (ECL) = Histamine
-Chief cells = Pepsinogen
-D cells = Somatostatin (Growth hormone)

158
Q

What are the 3 layers of the gut wall?

A

1.Muscularis Mucosae
2.Submucosa
3.Muscularis Externa

159
Q

What are Brunner’s glands and where are they located?

A

Submucosa of the duodenum that secrete alkaline mucous that counteracts acidity of chyme from stomach.

160
Q

What are Peyer’s patches and where are they located?

A

They are numerous lymphoid follicles located in the Submucosa of the ileum.

161
Q

What is Meissner’s Nerve Plexus and where is it located?

A

Controls motility, secretion rates and blood flow that is located in between muscle layers in the submucosa of the small intestine.

162
Q

What is Muscularis Externa and what type of muscle is it composed of?

A

-Muscle of the gut wall
-Smooth muscle (Inner circular and Outer Longitudinal)

163
Q

What innervates the Muscularis Externa?

A

Auerbach’s Plexus

164
Q

What is the difference between the Portal Vein and the Hepatic Vein?

A

The hepatic vein drains into the vena cava to carry blood out while the portal vein supplies the liver which is extremely high in nutrients.

165
Q

What 3 structures are present in the portal area of a liver?

A

-Hepatic Artery
-Hepatic Vein
-Bile duct

166
Q

What do you find throughout a Liver Lobule?

A

Sinusoids

167
Q

What are zones 1-3 in a liver lobule and how would a paracetamol overdoes affect them?

A

Zone 1: Hepatocytes closest to portal area and therefore receive plentiful O2 and nutrients.
Zone 2: Intermediate region receiving enough
Zone 3: Furthest away from portal area and closes to the central vein (major site for alcohol and drug detoxing) so low in O2 and nutrients.
*Therefore zone 3 is the most susceptible damage and in a paracetamol overdose those cells would die and create scarring of the liver.

168
Q

What are Kupffer cells and where are they located?

A

They are macrophages in the liver located on the inner walls of sinusoids.

169
Q

What are Bile canaliculus and how are they held in place?

A

Intracellular channels for the bile that are held together by Tight Junctions.

170
Q

What are the 4 types of cells present in the Islet of Langerhans in the pancreas and what do they secrete?

A
  1. a-cells = Glucagon
    2.B-cells = Insulin
    3.d-cells = Somatostatin (Growth hormone)
  2. F-cells = Pancreatic polypeptide
171
Q

Where is B12 stored?

A

Liver

172
Q

What is Pernicious Anaemia?

A

Lack of B12 caused red blood cells to be too big as Vit B12 is requied for cell division.

173
Q

How long till Pernicious anaemia develops?

A

Can be over a year as B12 can be stored in the liver for over a year

174
Q

How do Gallstones (Choleithiasis) occur?

A

Gallstones form when bile stored in the gallbladder hardens into stone-like material. This is caused usually by too much cholesterol but can also be due to high bile salts, or bilirubin (bile pigment).

175
Q

What is Steatosis?

A

Fatty change within the liver (accumulation of fatty droplets within the liver)
=Reversible cell injury

Note: You will see this in Non-Alcoholic Liver Disease

176
Q

What is Steatohepatitis?

A

-Accumulation of fat with accompanying inflammatory changes in the liver.
-Low grade chronic inflammation OR
-Bouts of hepatitis (mainly patients with alcohol abuse/addiction)
-Leads to fibrosis

177
Q

What causes steatohepatitis?

A

-High association with ALCOHOL
But also:
-Non-Alcoholic Fatty Liver Disease
-Medications/drugs

178
Q

How may Steatohepatitis affect alcohol abusers differently?

A

Instead of chronic inflammation can manifest as bouts of hepatitis.

179
Q

What does a FibroScan do?

A

Ultrasound probe used to measure :
-the stiffness of the liver (Elastography) as a marker for Fibrosis.
-the degree of fatty change (Steatosis) which is expressed as a CAP score

180
Q

How are the results of steatosis from a FibroScan expressed?

A

As a CAP score.

181
Q

What does Decompensated Liver Disease mean?

A

Acute deterioration in liver function in a patient with cirrhosis

182
Q

What are the characteristics of a patient with acute liver cirrhosis?

A

-Jaundice
-Coagulopathy = impaired synthesis of blood clotting factors
-Encephalopathy =due to hyperammonaemia
-Ascites = impaired albumin synthesis and portal hypertension
-Splenomegaly = portal hypertension
-GI bleeding = Oesophaegal varices

183
Q

What are the clinical signs of a patient with Chronic Liver Disease?

A

-Caput Medusa =Distended epigastric veins around umbilicus
-Splenomegaly = suggests portal hypertension
-Ascites = low albumin and increased portal hypertension
-Leukonychia = white fingernails
-Flapping tremor of outstretched hands (late sign)

184
Q

What does Leukonychia mean?

A

White finger nails

185
Q

What viruses can affect the Liver that are not Hepatotropic viruses (liver specific)?

A

-Herpes Simplex
-Epstein Barr Virus

186
Q

What is the mode of transmission for Hepatitis A?

A

Faecal - Oral

187
Q

How does HepA damage the liver?

A

Immune response to the virus does the actual damaging.

188
Q

Is Hep A acute or chronic?

A

Acute

189
Q

What is the incubation period for HepA?

A

2-6 weeks

190
Q

What does fulminant mean?

A

Severe and sudden onset

191
Q

What is the mode of transmission for Hepatitis B?

A

Blood, Sexual transmission

192
Q

Which Hepatitis viruses can have an asymptomatic carrier state?

A

Hep B

193
Q

What are the serious potential progressions of HepB?

A

5% with chronic Hepatitis lead to cirrhosis and then hepatocellular carcinoma.

194
Q

What is the mode of transmission for Hepatitis C?

A

Blood, contaminations (IV drug abusers, tattoos, haemophiliacs as a result of blood product contamination).

195
Q

Name examples of Autoimmune Liver Disease.

A

-Chronic Hepatitis
-Primary Biliary Cirrhosis (Cholangiopathy)
-Primary Sclerosing Cholangitis

196
Q

What is targeted and affected in Primary Biliary Cirrhosis?

A

Intrahepatic bile ducts

197
Q

What is targeted and affected in Primary Sclerosing Cholangitis?

A

Extrahepatic and Intrahepatic bile ducts

198
Q

What blood results would you expect from a patient with Autoimmune Hepatitis?

A

-Elevated serum IgG
-Positive autoantibodies (Anti-smooth muscle)
-No evidence of viral infection

199
Q

What other autoimmune disorders is Autoimmune Hepatitis associated with?

A

-Rheumatoid Arthiritis
-Thyroiditis
-Sjorgren’s syndrome
-Ulcerative colitis

200
Q

What age and gender are usually patients with Primary Biliary Cirrhosis?

A

(90%) Female
-Around 50yrs

201
Q

What other disease(s) is Primary Biliary Cirrhosis associated with?

A

-Sjogren’s syndrome
-Scleroderma
-Thyroid disease

202
Q

What antibody in particular would you expect to see in a patient’s blood test with Primary Biliary Cirrhosis?

A

Positive anti-mitochondrial autoantibodies

wham BAM I am the antibody
BAM:
(Primary)BILIARY(Cirrhosis)
Anti-Mitochondrial

203
Q

What are the key diagnostic tools for Primary Sclerosing Cholangitis?

A

MRI or ERCP which shows the chronic

204
Q

What other disease is Primary Sclerosing Cholangitis associated with?

A

Chronic IBD and Autoimmune Pancreastitis

205
Q

When is the common onset and what gene causes Haemochromatosis?

A

-Adult onset
-HFE

206
Q

Where do you find Peyer’s patches?

A

Throughout the GI tract but the majority of them are in the Ileum.

207
Q

What is the defining feature of the Jejunum in histology?

A

Longest Villi

208
Q

What are the 2 defining feature of the Large Intestine in histology?

A

1.Longest muscle (Teania Coli)
=3 longitudinal strips of smooth muscle

2.Lots of goblet cells (white spots) in the colonic crypts (glands)

209
Q

What post mortem feature of the large intestine makes it look like another part of the GI tract and why?

A

The villi contract so that they look like the Rugae from the stomach.

210
Q

What is a granuloma?

A

Tiny clusters of white blood cells (histiocytes - antigen presenting cells) due to inflammation or irritation. Instead of being phagocytotic, secretes cytokine that recruits more macrophages.
Note: It is not a cancer sign

211
Q

What are the histological findings of a patient with Chron’s Disease?

A

-Transmural inflammation = throughout
-breakdown of mucosa
-damage and inflammation goes into submucosa, muscularis externa and adventitia
-breakdown/ulceration of the epithelial layer
-muscularis externa becomes expanded and fibrotic

212
Q

What are the histological findings of a patient with Ulcerative Colitis ?

A

Breakdown of just mucosa and submucosa
-Lots of inflammatory cells in the submucosa
-Large blood vessels filled with blood in the mucosa

213
Q

What bacterias are possible to infect the biliary tree?

A

-Enterococcus species
-Enterobacteriaceae e.g E.coli, Salmonella (food poisening), Salmonella typhi (typhoid fever)

214
Q

What does Cholecystitis mean?

A

Inflammation of the gall bladder.

215
Q

What does Cholangitis mean?

A

Inflammation of the biliary tract.

216
Q

What are the characteristic symptoms of a biliary infection?

A

-Pain localising to right upper quadrant of abdomen
-Severe will have pain radiating to back
-Can also refer to shoulder tip on the right.
-Nausea
-Vomitting
-Fever
-Abdominal tenderness
-Can also present with sepsis

217
Q

What findings on abdominal examination would you find for a patient with a Biliary infection and why?

A

If the Biliary infection causes peritonitis:
-Abdominal tenderness
-Reflex guarding
-Rebound tenderness
-Muphy’s sign

218
Q

What is Murphy’s sign and what could it indicate?

A

When the examiner places their hand along the right costal margin, the patient cannot breath in comfortably.

-Can indicate a biliary infection (Acute Cholecystitis)

219
Q

If there are signs of sepsis in addition to a biliary tract infection, what antibodies should be given?

A

-Broad spectrum antibiotics : Beta Lactam / Beta-lactamase inhibitor
=Co-amoxiclav and Clavulanic acid

220
Q

Name a Beta Lactam antibody.

A

Co-amoxiclav

221
Q

Name a Beta-lactamase inhibitor .

A

Clavulanic Acid (aka Amoxicillin)

222
Q

What is an abscess?

A

Destruction of normal tissue due to infection and replacement of normal structure with pus and necrotic tissue.

223
Q

Why can’t antibiotics treat an abscess?

A

Due to their low pH, antibiotics can’t work till the pus has been drained.

224
Q

Which other parts of the body can spread their infection to the liver to create an abscess?

A

Appendix, Peritoneum, Colon or Gallbladder can spread to the liver via portal veins

225
Q

What is the treatment for an amoebic infection?

e.g Amoebic Dysentery

A

Metronidazole

226
Q

What type of bacteria is Leptospirosis caused by?

A

Leptospira interrogens
=Spirochetes spiral organisms

227
Q

What are the triad of symptoms for Leptospirosis?

A

Jaundice
Renal failure
Thrombocytopenia (deficiency of platelets in the blood. This causes bleeding into the tissues, bruising, and slow blood clotting after injury).

228
Q

What is the mode of transmission for Leptospirosis and who is mainly affected?

A

Rat urine contamination
-Sewage workers and Triathletes (swimmers)

229
Q

What is the incubation period for Leptospirosis?

A

1-2 weeks

230
Q

What is the prognosis for Leptospirosis?

A

90% resolve naturally after flu like symptoms.
- 5-10% have complications called Weil’s disease: Hepatitis, Jaundice, Haemorrhage and Meningitis

231
Q

What is Weil’s disease?

A

When a patient with Leptospirosis infection have complications such as Hepatitis.

232
Q

How to treat Weil’s disease?

A

Doxycycline

233
Q

How to diagnose Weil’s disease?

A

Serology

(=checking for antibodies in the blood)

234
Q

What blood markers would you expect from a patient with Hep A?

A

IgM

235
Q

What blood markers would you expect from a patient with Hep B?

A

Active / Chronic Infection:
-HBsAg
-HBeAg
note: E antigen indicates infectivity
Recent/Previous Infection :
-HB core Ab

Achieved immunity (via previous or vaccination):
-HB surface Ab

Viral load:
HB DNA PCR

236
Q

A patient has their blood test back with HBsAb present. What does that mean?

A

Past infection of Hep B and therefore have immunity

237
Q

What does the E antigen mean in patients with HepB?

A

Measure of infectivity

238
Q

How to treat Hep C?

A

Sofobuvir

239
Q

How does Viral Hepatitis affect ALP, AST and ALT?

A

ALP decreases
AST and ALT increase

240
Q

How do Antacids work?

A

They are weak alkalis that neutralise acid in the stomach and stimulates mucosal repair through Prostglandin release.

241
Q

What drug do Antacids negatively interact with?

A

Digoxin

(treat heart conditions)

242
Q

How do PPIs (e.g Omeprazole) work?

A

Inhibits protein pumps on parietal cells to stop H+ release in response to food.

243
Q

Why can’t you take Omeprazole when on Warafin?

A

Delays the elimination of Warafin

244
Q

When is Omeprazole prescribed?

A

-Reflux
-Duodenal and Gastric ulcers

245
Q

What exacerbates GORD?

A

Calcium channel blockers, Nitrates, Steroids, NSAIDs

246
Q

How can NSAIDs cause a peptic ulcer?

A

They inhibit Prostaglandin which protects the duodenum and stomach from gastric acid and pepsin.

247
Q

How to treat peptic ulcers?

A

H2 receptor antagonists (e.g Cimitidine) (for symptomatic relief) or PPIs

248
Q

What red flags require an urgent upper GI endoscopy?

A

-Chronic bleeding / Fe deficiency (anaemia)
-Weight Loss
-Dysphagia
-Persistent vomiting
-Persistent
-Dyspepsia (esp over 55 yrs)

249
Q

What two classes of drugs can cause constipation?

A

-Opioids e.g tramadol, oxycodone etc
-Anti-muscarinics e.g Atropine, Ipratropium Bromide

250
Q

What is the first line treatment for constipation?

A

-Fybogel (bulk-forming laxative)

251
Q

What is the contraindication for prescribing Fybogel?

A

If the patient is on opiods

252
Q

What should be prescribed for opioid induced constipation?

A

-Osmotic laxatives: Macrogels (Movicol)

-Also give a stimulant laxative:
Bisacodyl

253
Q

What other drug should be added on if a patient not only has constipation but the stool is hard?

A

Osmotic laxative: Movicol

254
Q

What is a bulk laxative?

A

Contains fibre to swell and distend the colon

255
Q

What is a stimulant laxative?

A

Agents that stimulate intestinal mobility

256
Q

What is an osmotic laxative?

A

Increases faecal bulk and moistens faeces by pulling water in

257
Q

What is Ascites?

A

Water distension in the peritoneum in the abdomen

258
Q

How do you treat Ascites?

A

-Spironalctone (correct Na+ inblance)
-Furosemide (to correct water retention)

259
Q

How to you treat Oesophageal Varices?

A

Phytomenadione (Vitamin K)
=stops varice bleeding for 6-8hrs)

260
Q

What organs are in the right hypochondrium region of the abdomen?

A

Liver
Gallbladder
Right Kidney

261
Q

What organs are in the epigastric region of the abdomen?

A

-Stomach
-Liver
-Pancreas
-Duodenum
-Spleen
-Adrenal glands

262
Q

What organs are in the left hypochondrium region of the abdomen?

A

-Stomach
-Left kidney
-Spleen
-Liver (tip)
-Pancreas

263
Q

What organs are in the right lumbar region of the abdomen?

A

-Small intestine
-Ascending colon
-Right kidney

264
Q

What organs are in the umbilical region of the abdomen?

A

Duodenum, Small intestine,
Transverse Colon

265
Q

What organs are in the left lumbar region of the abdomen?

A

Descending colon
Small intestine
Left kidney

266
Q

What organs are in the right iliac region of the abdomen?

A

Appendix
Cecum
Ascending colon
Small intestine

267
Q

What organs are in the suprapubic region of the abdomen?

A

Bladder
Sigmoid Colon
Reproductive organs

268
Q

What organs are in the left iliac region of the abdomen?

A

Sigmoid colon
Descending colon
Small intestine

269
Q

A patient is suffering pain in the right hypochondrium region. What are the possible causes?

A

-Hepatitis
-Heptatic Abscess
-Cholecystitis
-Cholangitis
-Gallstones

270
Q

A patient is suffering pain in the epigastric region. What are the possible causes?

A

-Gastritis
-GORD
-Peptic Ulcer
-Gastric perforation
-Gastroparesis
-Pancreatitis

271
Q

A patient is suffering pain in the left hypochondrium region. What are the possible causes?

A

-Pancreatitis
-Splenic Infarct
-Splenic Rupture
-Splenic Abscess

272
Q

A patient is suffering pain in the right lumbar region. What are the possible causes?

A

-Kidney stones
-Pyelonephritis
-Ulcerative Colitis

273
Q

A patient is suffering pain in the umbilical region. What are the possible causes?

A

GRAM:
-Gastroenteritis
-Rupture Abdominal Aorta Aneurysm
-Acute Small Bowel Obstruction (SBO)
-Mesentery Ischaemia

274
Q

A patient is suffering pain in the left lumbar region. What are the possible causes?

A

-Kidney stones
-Pyelonephritis
-Colitis

275
Q

A patient is suffering pain in the right iliac fossa region. What are the possible causes?

A

-Appendicitis
-Ulcerative Colitis
-Ovarian Torsion
-Tubo-ovarian abscess (TOA)
-Ovarian cyst

276
Q

A patient is suffering pain in the suprapubic region. What are the possible causes?

A

-Cystitis (inflammation of bladder due to infection)
-Pelvic Inflammatory Disease
-Sexually Transmission Infection (STIs)
-Ectopic Pregnancy

277
Q

A patient is suffering pain in the left iliac fossa region. What are the possible causes?

A

-Colitis
-Diverticulitis
-Ovarian Torsion
-Tubo-Ovarian Abscess (TOA)
-Ovarian Cyst

278
Q

At what point does the Abdominal aorta enter the abdominal cavity and divide?

A

T12

279
Q

At what point does the abdominal aorta terminate?

-Mention bony landmark as well as landmark structures.

A

At the common iliac arteries at L4.

280
Q

What are the 3 branches of the abdominal aorta when it divides in the abdomen?

A

1.Coeliac trunk
2.Superior mesentery
3.Inferior mesentery

281
Q

What does the coeliac trunk divide into?

A

1.Left gastric
2.Splenic
3.Common Hepatic

282
Q

Is the stomach retroperitoneal or intraperitoneal?

A

Intraperitoneal

283
Q

What does the common hepatic artery divide into?

A

1.Gastroduodena2.Right Gastric
3.Right Gastro-omental

284
Q

What is the difference between mesentery and omenta?

A

Mesentary is connective tissue with arteries etc, while omenta is just CT to attach organs to the abdominal wall

285
Q

Where does the Superior Mesenteric Artery appear from the Abdominal aorta?

A

L1

286
Q

What does the Superior Mesenteric Artery split into?

A

1.Middle Colic Artery
2.Right Colic Artery
3.Illeocolic artery
4.Jejunal and ileal arteries

Way to remember:
MRI II

287
Q

Name the parts of the large intestine.

A

-Ascending Colon
-Transverse Colon
-Descending Colon
-Sigmoid Colon

288
Q

Where does the Ascending colon lie?

Note: Is it retro- or intra-peritoneal?

A

Retroperitoneal ascending from the cecum to the right lobe of the liver.

289
Q

What is the right colic flexure?

A

Where the ascending colon turns right at the right liver lobe and goes into the transverse colon

290
Q

Where does the transverse colon lie?

A

From the right colic flexure to the spleen.

291
Q

What is the left colic flexure?

A

Where the transverse colon turns downwards at the spleen to go into the Descending colon.

292
Q

Where does the descending colon lie?

(Note: Is it Retro- or Intra-peritoneal)

A

Retroperitoneal but passes over the left kidney, travelling from the left colic flexure to the pelvis

293
Q

Where does the sigmoid colon lie?

A

In the left lower quadrant of the abdomen extending from the left iliac fossa to the S3 vertebra.

294
Q

What allows the sigmoid colon to be more mobile than the rest of the large bowel?

A

The mesentery called Sigmoid Mesocolon which is a long length.

295
Q

How is the pancreas supplied?

A

By the pancreatic branches of the Splenic artery

296
Q

What are the parts of the pancreas?

A

-Head
-Ucinate process (projects off the head)
-Neck
-Body
-Tail

297
Q

What are the 2 HIV tests?

A

-HIV 1 & 2 Antibody test
-HIV p24 Antigen test

298
Q

When can you test for HIV 1&2 antibodies?

A

3-12 weeks after exposure

299
Q

Where do you usually see HIV 1 infections in the world?

A

USA

300
Q

Where do you usually see HIV 2 infections in the world?

A

Africa

301
Q

When can you do a HIV p24 test?

A

In the first few weeks after exposure

302
Q

What is the HIV p24 test?

A

Present in acute HIV infection in the first weeks of exposure to HIV, the body produces p24 antigen

303
Q

What does Seroconversion mean?

A

Process of developing specific antibodies in the blood as a result of infection / immunisation

304
Q

What is the difference between compensated and decompensated Liver Cirrhosis?

A

Compensated is when the Liver is still working and Decompensated is when the Liver isn’t .

305
Q

What symptoms should you expect from a patient with Compensated Liver Cirrhosis?

A

-Fatigue and weakness
-Poor apetite
-Weight loss
-Nausea / vomiting
-Mild pain / discomfort in upper right quadrant of abdomen
-Fever

Note: you only get the serious signs in decompensated cirrhosis

306
Q

What symptoms should you expect from a patient with Decompensated Liver Cirrhosis?

A

-Jaundice
-Portal Hypertension
(Ascites, Hepatic Encephalopathy, Varices)
-Hepatorenal syndrome

307
Q

What are the 4 most common causes of Liver Cirrhosis?

A

-Alcohol related liver disease
-Non-alcoholic fatty liver disease
-Hep B
-Hep C

308
Q

What can indicate Hepatocellular Carcinoma?

(Note that it won’t always show up)

A

-Raised Serum Alpha Fetoprotein

309
Q

How does Hepatocellular carcinoma develop from Liver Cirrhosis?

A

Cirrhosis has premalignant lesions of dysplastic nodules that can progress to HCC.

310
Q

What are the 3 main Liver autoimmune conditions to know about?

A

-Autoimmune Hepatitis
-Primary Sclerosing Cholangitis
-Primary Biliary Cirrhosis

311
Q

What would you expect from a Liver Profile for a patient with Autoimmune Hepatitis?

A

Hepatic picture:
-High ALT and AST
-Minimal change in ALP

-Autoantibodies

312
Q

What autoantibodies would you expect for type 1 Autoimmune Hepatitis?

A

-Anti-Nuclear Antibodies (ANA)
-Anti-smooth muscle antibodies (Anti​ actin)
-Anti-soluble liver antigen (anti-SLA/LP) ​

313
Q

What is a typical patient of Type 1 Autoimmune Hepatitis?

A

Post-Menopausal women in 40s-50s

314
Q

What autoantibodies would you expect for type 2 Autoimmune Hepatitis?

A

-Anti-liver kidney microsomes 1 (anti-​LMK1)
-Anti-liver cytosol antigen type 1 (anti-​ LC1)

                                                 ​
315
Q

What would you expect from a Liver Biopsy for Autoimmune Hepatitis?

A

Interface Hepatitis = Death of hepatocytes at the interface of parenchyma and the connective tissue of the portal zone, accompanied by a variable degree of inflammation and fibrosis.​

​

316
Q

What treatments would be offered to a patient with Autoimmune Hepatitis?

A

-High dose steroids -Prednisolone
-Immunosuppressants -Azatioprine

317
Q

What is Primary Sclerosing Cholangitis?

A

Intrahepatic and Extrahepatic Bile ducts become inflamed and damaged developing strictures that obstruct bile flow out of the liver and into the intestines. Chronic obstruction leads to hepatitis , fibrosis and cirrhosis.

318
Q

What does Sclerosis mean?

A

Stiffening and hardening of bile

319
Q

What does Cholangitis mean?

A

Inflammation of bile ducts

320
Q

What is Primary Sclerosing Cholangitis highly related to?

A

Ulcerative Colitis
(70% of patients have both)

321
Q

What is a typical patient with Primary Sclerosing Cholangitis?

A

Male, 30-40s (with Ulcerative Colitis)

322
Q

What is the clinical presentation of a patient with Primary Sclerosing Cholangitis?

A

-Pruritus ​

-Jaundice​

-Right Upper Quadrant pain (Right Hypochondrium/Epigastric region)​

-Hepatomegaly​

-Splenomegaly ​

323
Q

What investigations should be done for a suspected Primary Sclerosing Cholangitis patient?

A

-Liver profile
-Magnetic Resonance Cholangiopancreatography (MRCP)
-Colonoscopy (check for ulcerative colitis)

324
Q

What liver profile results would you expect from a patient with Primary Sclerosing Cholangitis?

A

Obstructive picture:
-High ALP
-High bilirubin (later in disease)

325
Q

What does an obstructive picture mean with a liver profile?

A

High ALP (and high bilirubin later in disease)

326
Q

What would you see in an MRCP for a patient with Primary Sclerosing Cholangitis?

A

Bile duct strictures

327
Q

What treatments would be offered for a patient with Primary Sclerosing Cholangitis?

A

-No cure
-ERCP for dominant strictures to insert a stent
-Colestryamine for Pruritus

328
Q

What are possible complications of Primary Sclerosing Cholangitis?

A

Colorectal cancer (in patient with UC as well)​

Cholangiocarcinoma develops in 10-20% of cases​

Fat soluble vitamin deficiencies (Vit A,D,

329
Q

What is Primary Biliary Cholangitis/Cirrhosis ​?

A

Intrahepatic ducts are attacked by immune system causing inflammation and damage to the epithelial cells of the bile ducts leading to obstruction of bile flow and therefore Cholestasis (reduced bile flow). This can lead to liver fibsosis, cirrhosis and failure.​

330
Q

What is a typical patient with Primary Biliary Cholangitis/Cirrhosis ​?

A

Caucasian, Women, 40-60yrs

331
Q

Describe a clinical presentation of a patient with Primary Biliary Cholangitis/Cirrhosis ​?

A

-Pruritus ​

-Jaundice​

-Abdominal pain​

-Hepatomegaly​

-Pale,greasy stools ​

-Dark urine ​

-Xanthoma (cholesterol deposits)

332
Q

What investigations should be done for a suspect Primary Biliary Cholangitis/Cirrhosis ​?

A

-Liver profile
-Liver Biopsy

333
Q

What would you expect from a Liver profile from a patient with Primary Biliary Cholangitis/Cirrhosis ​?

A

-Obstructive picture:
=High ALP (high bilirubin later in disease)

-Autoantibodies

334
Q

What autoantibodies would you expect in a patient with Primary Biliary Cholangitis/Cirrhosis ​?

A

-Anti-mitochondrial antibodies (AMA) = most specific to PBC patients ​

-Anti-nuclear antibodies

335
Q

What would you expect from a Liver Biopsy from a patient with Primary Biliary Cholangitis/Cirrhosis ​?

A

Granulomas​

Portal based inflammation – portal tracts composed of lymphocytes ​

​

336
Q

What treatments would be offered to patients with Primary Biliary Cholangitis/Cirrhosis ​?

​

A

-Ursodeocycholic acid (protect cholangiocytes from damage)

-Colestryamine (treat Pruritus)

337
Q

What are the possible complications of Primary Biliary Cholangitis/Cirrhosis ​?

A

Liver Cirrhosis​

Hepatocellular Carcinoma ​

Fat soluble vit deficiency (A,D,E and K) ​

Thyroid Disease ​

338
Q

What drugs are contraindicated in hepatic dysfunction?

(remember mneumonic)

A

Alan Calls Dave Avoiding Martin’s Ratty Egotistical Pessimism Very Quietly

Amiodarone
Chlorpromazine
Diclofenac
Anabolic steroids
Methotrexate
Rifampin
Erythromycin
Phenytoin
Valproate
Quinidine

339
Q

What is the treatment for HepB?

A

Usually clears up on its own WITHOUT treatment

340
Q

What is the Myenteric Plexus?

A

The myenteric plexus lies in between the outer longitudinal and inner circular smooth muscle layers of the intestines. By stimulating these muscles, it controls motility along the gastrointestinal tract.

341
Q

What blood results would you expect from a patient with Jaundice due to Pre-Hepatic causes?

A

-High T.Bilirubin
-SLIGHT raised AST and ALT

342
Q

What blood results would you expect from a patient with Jaundice due to Intra-Hepatic causes?

A

-ALT and AST raised results will be MUCH higher than ALP and GGT raised results.

343
Q

What blood results would you expect from a patient with Jaundice due to Post-Hepatic causes?

A

-ALP and GGT raised results will be MUCH higher than ALT and AST raised results.

344
Q

What does Vertical transmission of Hep B mean?

A

Vertical transmission of HBV is defined as positivity at 6–12 months of life of the hepatitis B surface antigen (HBsAg) or of HBV-DNA in an infant born to an infected mother

345
Q

What is Acetaminophen?

A

aka Paracetamol
(=non-opiod analgesic)

346
Q

What does high does of acetaminophen do?

A

Liver damage - Medical emergency!

347
Q

What is the treatment for a acetaminophen overdose?

A

IV fluids
Antidotal therapy - N-acetylcysteine (Acetadote, Mucomyst)

348
Q

What factors/illnesses can give you a higher likelihood to get drug-induced hepatitis?

A

-Diabetes
-Pregnancy
-Smoking and Alcohol

349
Q

What is the most common drug responsible for drug induced liver injury in the world?

A

Amoxicillin-Clavulonate

350
Q

What are the drugs to know about that can cause drug induced liver injury.

A

-Diclofenac
-Naproxen
-Amiodarone
-Anabolic steroids
-Methotrexate
-Methyldopa
-Statins
-Erythromycin
-Birth control pills

351
Q

What 2 antibiotics are most implicated in liver damage?

A

Amoxicillin/Clavulanic acid
Flucloxacillin
Erythromycin

352
Q

Where does the gallbladder lie?

A

Anterior to the duodenum and below and behind the liver

353
Q

Where the is most common location of gallstones?

A

Hartmann’s pouch
(the mucosal folds of the neck of the gallbladder)

354
Q

Describe the anatomy of the gall bladder.

A

Fundus - round portion that projects into the interior surface of the liver

Body- largest part of the gallbladder

Neck- where the gallbladder tapers to become continuous with the cystic duct leading into the biliary tree

355
Q

Describe the pathway of bile through the biliary tree.

A

1.Newly synthesised from the liver secreted from hepatocytes and drains from both lobes of liver via CANILICULI, INTRALOBULAR DUCTS and COLLECTING DUCTS into LEFT and RIGHT HEPATIC DUCTS.

2.Those ducts merge to form the COMMON HEPATIC DUCT which runs along the HEPATIC VEIN

3.As the COMMON HEPATIC DUCT descends it merges with the CYSTIC DUCT to form the COMMON BILE DUCT

4.It is then joined by the MAIN PANCREATIC DUCT to form the HEPATOPANCREATIC AMPULLA

5.This empties into the duodenum via the MAJOR DUODENAL PAPILLA

356
Q

What is the sphincter of oddi?

A

The muscular valve of the major duodenal papilla where the bile empties into the duodenum

357
Q

What merges to form the Common Hepatic Duct?

A

CANILICULI, INTRALOBULAR DUCTS and COLLECTING DUCTS

358
Q

What merges to form the Common Bile Duct?

A

The Common Hepatic Duct and the Cystic Duct.

359
Q

What merges to form the Hepatopancreatic Ampulla?

A

Common Bile Duct and the Main Pancreatic Duct.

360
Q

Where is bile made and where is it stored?

A

Made in the Liver
Stored in the Gallbladder

361
Q

What supplies the gallbladder?

A

The Cystic Artery

(branch from the right hepatic artery which came from the common hepatic artery which came from the coeliac trunk)

362
Q

What is Charcot’s Triad?

A

-Upper Quadrant Pain
-Fever
-Jaundice

=Typical of Cholangitis

363
Q

What is the definition of Biliary Colic?

A

-Right upper quadrant pain FOLLOWING A FATTY MEAL
(due to the contraction of the gall bladder)

=Gallstones

364
Q

When would a physician think of Cholangiocarcinoma as a possible diagnosis? What is the red flag symptom / test result?

A

-Painless Jaundice
-Obstructive Liver Profile picture (without pain)

365
Q

What presentation would you usually suspect for a patient with drug induced liver damage?

A

-Abnormal liver profile (usually obstructive)
-Jaundice
-No pain (usually)

366
Q

What is Trimethorprim?

A

Antibiotic usually used to treat UTIs.

367
Q

What is Hepatic Encephalopathy?

A

Brain dysfunction caused by advanced liver failure.

368
Q

What type of tremor would you see in a patient with advanced liver damage?

A

-Liver flap
-Asterixis
-Coarse tremor (very noticable)

369
Q

A patient has suspect Cirrhosis but their ALT is normal. How may this change the diagnosis?

A

It doesn’t! Patients with Cirrhosis can have normal ALT.

370
Q

What are the Interstitial Cells of Cajal?

A

Native pacemakers of the myenteric system stimulating the smooth muscle wall of the intestine.

Consolidation by CBL (3 decks)

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