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Year 2 > Case 3 > Flashcards

Case 3 Flashcards

1
Q

Dependence syndrome

A

3 or more of the following symptoms:

withdrawal state
evidence of tolerance 
lack of control
strong desire 
neglect of alternative interests 
persist despite harmful consequences
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2
Q

Negative reinforcement behaviours

A

Relief of bad symptoms - starting to drink alcohol again due to unpleasant withdrawal symptoms

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3
Q

Positive reinforcement behaviours

A

Bring about good symptoms - drinking alcohol for euphoric feeling of being intoxicated

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4
Q

How does smoking bring about release of dopamine?

A

Nicotine binds to nicotinic (ACh) receptors in mesolimbic reward system. Activation of dopamine cells = release of dopamine.

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5
Q

Dopamine pathway is involved in…

A

Reward, pleasure and euphoria

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6
Q

Serotonin pathway is involved in…

A

Mood
Memory
Sleep
Cognition

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7
Q

Mallory Weis Syndrome

A

Gastro-oesophageal laceration due to alcoholism, bulimia or any other condition causing violent vomiting.

Causes painful haematemesis.

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8
Q

Korsakoff’s Syndrome

A

Persistent amnesia due to chronic alcoholism

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9
Q

Transmission of Hep A

A

Faeco oral

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10
Q

Risk factors for Hep A

A

Poor sanitation
Gay men
Travellers

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11
Q

Prevention of Hep A

A

Vaccination
Hand washing
Food/water hygiene

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12
Q

Hepatitis E

A

Very similar to Hep A but very rare.

Associated with animal contact.

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13
Q

Treatment for Hep A

A

No specific treatment - spontaneous clearance by immune system.

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14
Q

Signs/Symptoms of Hep A

A

Fever
Malaise
Jaundice

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15
Q

Transmission of Hep B

A

Blood (assoc with needle stick injury and IV drug use)
Sexual (semen)
Vertical

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16
Q

Acute Hep B can become chronic, what is the chance of HBV becoming chronic?

A

95% in neonates

<5% in adults

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17
Q

Definition of chronic HBV

A

Failure to clear after 6 months

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18
Q

Effects of chronic HBV

A

End stage liver disease - portal hypertension/ascites, bleeding oesophageal varices, liver failure

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19
Q

Vaccination is available for which forms of hepatitis

A

A and B

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20
Q

Transmission of Hep C

A

Blood and vertical

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21
Q

Acute Hep C can become chronic. What is the chance of Hep C becoming chronic?

A

85% (15% will recover)

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22
Q

What is the risk of liver cirrhosis in Hep C?

A

20%/year of individuals with Hep C will get cirrhosis of the liver

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23
Q

Hepatitis D

A

Only presents WITH Hep B

Very high incidence of cirrhosis development

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24
Q

Features of liver cirrhosis

A 
Ascites and oedema 
Impaired immunity 
Oesophageal Varices 
Splenomegaly 
Testicular atrophy 
Gynaecomastia 
Spider Naevi
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25
Q

Why does liver cirrhosis cause oedema?

A

Low albumin

Increased hydrostatic pressure of blood

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26
Q

Why does liver cirrhosis cause ascites?

A

Low albumin

Portal hypertension

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27
Q

Why does liver cirrhosis cause oesophageal varices and splenomegaly?

A

Portal hypertension

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28
Q

Why does liver cirrhosis cause Testicular atrophy and Gynaecomastia

A

Impaired metabolism of oestrogen

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29
Q

HBcAg

A

Core antigen

Present during acute infection

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30
Q

HBsAg

A

Surface antigen

Present during active infection

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31
Q

HBsAb

A

Surface antibody

Present in an immune person

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32
Q

HBcAb

A

Core antibody
Present in someone who has had the infection in the past.

Does not provide immunity

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33
Q

How is vertical transmission of HBV prevented?

A

Antiviral therapy to mother during pregnancy.
Passive immunisation of mother (eAg)
Vaccination of infant (3 dose schedule, started at birth)

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34
Q

Oesophageal varices

A

Dilated submucosal veins at anastomosis between systemic and portal drainage of oesophagus.
Usually caused by portal hypertension.
Risk of bleeding - causing haematemesis

High risk in alcoholics

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35
Q

Symptoms of GORD

A

Heartburn
Dysphagia
Sour taste in mouth

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36
Q

Causes of GORD

A

Dysfunction of lower oesophageal sphincter
Hiatus Hernia
Delayed gastric emptying (functional dyspepsia)

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37
Q

Sliding hiatus hernia

A

Diaphragm no longer supporting lower oesophageal sphincter.

Upper part of stomach can slide through.

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38
Q

Rolling hiatus hernia

A

Part of stomach herniates into chest next to normal oesophagus.
Looks like a balloon next to oesophagus.

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39
Q

Barrett’s Oesophagus

A

Metaplasia of lower oesophageal squamous epithelium to gastric columnar due to chronic acid exposure.
Can lead to adenocarcinoma

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40
Q

How is cholesterol converted to bile salts?

A

Cholesterol converted to bile acids by Cytochrome P450.

Bile acids are conjugated to glycine or taurine by liver cells to form bile salts.

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41
Q

Primary vs secondary bile salts

A

Primary - formed by hepatocytes

Secondary - formed by bacteria in the intestine

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42
Q

How are bile salts recycled?

A

Absorbed in GI tract and enter portal circulation.

Active reuptake of bile salts from blood into liver cells via sodium dependent transporters

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43
Q

HMG CoA Reductase

A

Enzyme responsible for cholesterol synthesis.

Inhibited by statins.

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44
Q

Bilirubin Metabolism

A

Haem from Hb split into Fe2+ and Porphyrin ring.
P ring converted to biliverdin which is converted to bilirubin.
Bilirubin is conjugated by the liver and converted to urobilinogen.
Urobilinogen is excreted in urine or converted to stercobilin to be removed in faeces.

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45
Q

Conjugation of bilirubin

A

UDP-glucuronic acid supplies glucuronic acid, leaving UDP remaining.
Bilirubin also loses albumin

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46
Q

Signs/Symptoms of jaundice

A

Dark urine - excretion of bilirubin via kidneys
Pale stools with fatty streaks (absence of bilirubin and poor fat digestion)
Itching (accumulation of bile acids)

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47
Q

Conjugated bilirubin converted to urobilinogen by…

A

Bacterial flora of the colon.

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48
Q

Function of LDL

A

Carries cholesterol from liver to tissues

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49
Q

Function of HDL

A

Carries cholesterol from tissues to liver

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50
Q

Length of thoracic oesophagus

A

23cm

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51
Q

Length of abdominal oesophagus

A

2cm

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52
Q

Muscle distribution in oesophagus

A

Superior 1/3 = Voluntary striated
Middle 1/3 = mixture
Inferior 1/3 = smooth muscle

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53
Q

Vertebral level of oesophageal hiatus

A

T10

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54
Q

Greater curvature of stomach is supplied by

A

Short gastric arteries

Right and left omental arteries

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55
Q

Lesser curvature of the stomach is supplied by

A

Left gastric artery

Right gastric branch of hepatic artery

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56
Q

Epiploic foramen

A

Allows communication between greater and lesser sac

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57
Q

Lesser omentum

A

Connects stomach to duodenum and liver

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58
Q

Function of Greater omentum

A

Involved in combating GI infection - contains many lymph nodes with macrophages

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59
Q

Parasympathetic innervation of stomach

A

Vagus nerve

Increased stomach motility, gastric juice secretion and relaxation of sphincter

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60
Q

Sympathetic innervation of stomach

A

Coeliac plexus

Reduced stomach motility and gastric juice secretion. Constriction of sphincters

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61
Q

Transition from foregut to midgut occurs at…

A

Major Duodenal Papilla in superior duodenum

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62
Q

Distinguishing features of jejunum

A

Red
Thick walled
Long vasa recta (straight arteries)
Less arcades (arterial loops)

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63
Q

Distinguishing features of ileum

A

Pink
Thin walled
Short vasa recta
More arcades

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64
Q

Primary site of lipid absorption

A

Jejunum

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65
Q

Primary site of bile salt absorption

A

Ileum

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66
Q

Primary site of cobalamin (Vit B12) absorption

A

Ileum

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67
Q

LFTs: Elevated ALP - Alkaline Phosphatase

A

When bile flow is obstructed or biliary tree is damaged

When canaliculi or hepatocytes are damaged

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68
Q

LFTs Elevated AST - Aspartate Transaminase

A

When hepatocellular necrosis occurs BUT also in heart, muscle, kidney and brain injury

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69
Q

LFTs: Elevated ALT

A

A more specific measure than AST. Only increased with liver failure

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70
Q

LFTs: Low albumin indicates…

A

Chronic liver disease - reduced synthetic capability of liver.

OR

Inflammation - redistribution of albumin into extracellular space of plasma compartment

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71
Q

LFTs: Prothombin time

A

More sensitive indicator than albumin since clotting factors have a shorter half life.
Elevated PT in chronic liver dysfunction

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72
Q

Causes of prehepatic unconjugated hyperbilirubinaemia

A 
Haemolytic anaemia 
Defects in RBC membranes 
Defects in Hb production 
Sickle cell anaemia 
Defect in RBC metabolism
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73
Q

Mechanism for prehepatic unconjugated hyperbilirubinaemia

A

Bilirubin is produced at a greater rate than the capacity of the liver to conjugate it.
i.e. excessive breakdown of RBCs

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74
Q

Lab results for prehepatic unconjugated hyperbilirubinaemia

A 
Raised plasma unconjugated bilirubin.
Normal conjugated bilirubin (since liver is functioning normally)
Raised reticulocytes (immature RBCs)
Low Hb 
Normal LFTs
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75
Q

Mechanism for Hepatic unconjugated hyperbilirubinaemia

A

Reduced conjugated and excretion of bilirubin

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76
Q

Causes of Hepatic unconjugated hyperbilirubinaemia

A

Crigler Najjar Syndrome - lack of conjugating enzyme
Gilbert’s - mild deficiency of conjugating enzyme
Newborns with immature liver.

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77
Q

Lab results for hepatic unconjugated hyperbilirubinaemia

A

Raised plasma unconjugated bilirubin
No urinary conjugated bilirubin
Raised AST, ALP and GGT

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78
Q

LFTs: Gamma-Glutamyl Transferase

A

Found almost exclusively in the liver

Increased during cholestasis or hepatocellular disease

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79
Q

Mechanism for hepatic conjugated hyperbilirubinaemia

A

Liver damage leading to reduced uptake of unconjugated bilirubin from plasma

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80
Q

Causes of hepatic conjugated hyperbilirubinaemia

A

Viral or toxic hepatitis or cirrhosis causing leakage of bilirubin from hepatocytes.
Dubin-Johnson Disease (deficiency in conjugated bilirubin transport into canaliculi)

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81
Q

Lab results in hepatic conjugated hyperbilirubinaemia

A

Raised plasma conjugated bilirubin (leaking out of hepatocytes)
Raised urine conjugated bilirubin and urobilinogen
Raised ALT and AST

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82
Q

Causes of post-hepatic conjugated hyperbilirubinaemia

A 
Gall stones 
Biliary stricture 
Cancer 
Biliary cirrhosis 
Drugs 
Acute hepatocellular damage e.g. infection
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83
Q

Lab results for post-hepatic conjugated hyperbilirubinaemia

A

Elevated plasma and urine conjugated bilirubin
No urobilinogen (since bilirubin cannot leave liver)
Raised ALP, AST, ALT and GGT

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84
Q

Cholesterol based gall stones

A

80% of cases
Occur when bile contains too much cholesterol and too little bile salts
Less calcium
Green/Brown in colour

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85
Q

Pigment gall stones

A

20% of cases
Composed of bilirubin pigment and calcium salts.
Small and dark

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86
Q

Risk factors for cholesterol gall stones

A

Increased cholesterol - female, increased age, obesity

Increased bile salts - high oestrogen, malabsorption

87
Q

Risk factors for pigment gall stones

A

Increased RBC breakdown (e.g. sickle cell anaemia) - causing increased unconjugated bilirubin.
Chronic biliary infected - causing glucuronidase production by epithelium or bacteria.

88
Q

Hartmann’s Pouch

A

Mucosal fold at neck of gallbladder

Common site for gallstones to become lodged.

89
Q

Symptoms of gallstone lodged in common hepatic bile duct

A

Post-hepatic Conjugate Hyperbilirubinaemia

Dark urine, pale stools, yellow skin, fatty streaks in stool.

90
Q

Symptoms of gallstone lodged in Ampulla of Vater

A

Post-hepatic Conjugate Hyperbilirubinaemia
Dark urine, pale stools, yellow skin, fatty streaks in stool

Plus pain in abdomen and back due to pancreatitis.

91
Q

Acute Pancreatitis

A

Blockage of duct causing injury to acini cells since activated digestive enzymes are trapped in pancreas.

92
Q

Symptoms of Chronic Pancreatitis

A

Steatorrhoea

Flatulence and fowl smelling stools (inability to digest proteins, bacterial growth in intestines)

93
Q

Acinar cells of pancreas release…

In response to…

A 
Pancreatic enzymes (protease, amylase and lipase)
Cl- rich secretions

In response to CCK

94
Q

Ductal cells of acini of pancreas release…

In response to…

A

HCO3- (exchanged for Cl- released by acinar cells)

In response to secretin and ACh

95
Q

How does Secretin bring about alkaline secretions from pancreatic acinus?

A 
Activates Gs (GPCR)
PKA activated
PKA phosphorylates Cl- channels (cAMP mediated CFTR).
Stimulates HCO3-/Cl- exchange by ductal cells.
Cl- in lumen exchanged for HCO3- in ductal cells
96
Q

CFTR Channel

A

Cystic Fibrosis Transmembrane Conductance Regulator (encoded by CFTR gene)
Transport of Cl- across apical membrane of acini.
Regulated by cAMP
Ca2+ dependent.

97
Q

Hormonal and neural control mechanisms involved in CEPHALIC phase of digestion

A

Cephalic phase accounts for 30% digestion.

Sight, taste and smell of food stimulates output of gastric glands (via parasympathetic afferents)
Stimulates output of gastric glands.
Increased watery saliva production, containing amylase and mucins (stimulated by bradykinin and kallikrein)
Release of zymogen granules from acinar cells in pancreas.

98
Q

Hormonal and neural control mechanisms involved in GASTRIC phase of digestion

A

Gastric phase accounts for 60% of digestion.

Distension of stomach and chemical content of food results in gastrin production from G cells.
Also stimulates vago-vagal gastropancreatic reflex i.e. Pancreatic acini release digestive enzymes and alkaline fluid.
Gastrin also stimulates acinar cells.

99
Q

Hormonal and neural control mechanisms involved in INTESTINAL phase of digestion

A

Intestinal phase accounts for 5% of digestion.
pH of 2-3 in duodenum due to stomach acid stimulates S cells to secrete secretin.
Secretin (and H+ and GIP) stimulates D cells to produce somatostatin.
Somatostatin inhibits G cells (therefore, less Gastrin)
Secretin causes duct cells in pancreatic acini to secrete bicarbonate.

CCK released from duodenal cells in response to products of protein and fat digestion. CCK stimulates acinar cells of pancreas to secrete enzyme rich fluid.

100
Q

Proteolytic component of pancreatic secretions

A

Trypsin, chymotrypsin and elastase (endopeptidases)

Carboxypeptidases (attack terminal bond)

101
Q

Liplytic component of pancreatic secretions

A

Colipase, cholesterol esterase and PLA2 secreted as zymogens.

102
Q

What is the significance of trypsin in exocrine pancreatic secretions?

A

Activates zymogen granules of all proteolytic and lipolytic pancreatic secretions.
Activated by enteropeptidase.

103
Q

Cholagogue

A

Promotes discharge of bile

104
Q

Orexin is released from…

In response to …

A

Released from lateral and posterior hypothalamus

In response to low blood glucose and high ghrelin.

105
Q

Ghrelin is released from…

In response to…

A

Released from gastric mucosa of stomach and small intestine.

In response to empty stomach, hypoglycaemia

106
Q

Leptin is released from…

In response to…

A

Released from adipocytes

In response to distension of stomach and presence of glucocorticoids (insulin)

107
Q

Leptin is responsible for…

A

Suppression of appetite
Brown fat metabolism
Maintenance of baseline weight

108
Q

CCK is released from…

In response to…

A

released from I cells in duodenal mucosa.

In response to products of protein and fat digestion in duodenum

109
Q

CCK is responsible for…

A

Suppression of appetite
Slowing of gastric emptying
Contraction of gallbladder

110
Q

PYY is released from…

In response to…

A

Released from L cells in colon and ileum.

In response to calorie intake

111
Q

PYY is responsible for..

A

Suppression of appetite

Slowing of peristalsis to maximise absorption.

112
Q

Cause of fatty change in the liver

White droplets

A

Metabolic stress
Alcohol
Pregnancy

113
Q

Liver change which occurs as a result of cholestatic obstruction

A

Proliferation of bile ducts

Also occurs as a result of autoimmune disease, viral hepatitis, pregnancy and some drugs.

114
Q

Hepatocyte necrosis

A

Affects individual cells, usually in zone 3 of liver acini (poorer blood supply)
Cells have a shrunken nucleus

115
Q

How does liver fibrosis differ from cirrhosis?

A

Fibrosis results from inflammation and is reversible.

Cirrhosis results from repetitive injury and is irreversible.

116
Q

Why is liver at a high risk of metastatic cancer?

A

Dual blood supply

117
Q

Drugs which can cause dose-dependent liver damage

A

Paracetamol (in over dose) - zone 3 necrosis

Methotrexate - fibrosis

118
Q

Glisson’s Capsule

A

Fibrous layer coating the liver

119
Q

Falciform ligament

A

Attaches anterior surface of liver to anterior abdominal wall
Free edge contains ligamentum teres (remnant of umbilical vein)

120
Q

Lobes of the liver

A

Left
Right
Quadrate (anterior)
Caudate (posterior)

121
Q

Morrison’s Pouch

A

Hepatorenal recess - most likely place for fluid collection in a bed-ridden px

122
Q

Blood supply to the liver:

A

Hepatic artery proper - branch of coeliac trunk carrying oxygenated blood.

Hepatic portal vein - carries deoxygenated blood containing nutrients absorbed from small intestine (Dominant blood supply to parenchyma

123
Q

Autonomic nerve supply to liver

A

Parasympathetic - vagus nerve

Sympathetic - coeliac plexus

124
Q

Sphincter of Oddi

A

Opening of hepatopancreatic Ampulla of Vater into duodenum.

125
Q

Vasculature of gallbladder

A

Arterial supply - cystic artery (branch of common hepatic)

Venous drainage - cystic vein (drains into portal vein)

126
Q

Autonomic innervation of gallbladder

A

Sympathetic - coeliac plexus

Parasympathetic - vagus nerve

127
Q

Epithelium which lines the gall bladder

A

Simple columnar

128
Q

Connective tissue on the outer surface of the gallbladder

A

Adventitia - where GB attaches to liver

Serosa - at free edge

129
Q

Serosa

A

Encloses body cavities. Consists of a thin layer of connective tissue and a layer of cells secreting serous fluid.

130
Q

Adventitia

A

Thin layer of connective tissue

131
Q

Function of myenteric plexus

A

Motor innervation of GI tract.

132
Q

Function of submucosal plexus

A

Carries sensory information from stretch receptors

Regulates secretory activity of the GI tract.

133
Q

Effects of perforation of oesophagus

A

Contents extravasates into mediastinum.

Causes breathing difficulties and lung infection.

134
Q

Epithelium found in the stomach

A

Simple columnar

135
Q

Distribution of mucosa in the stomach

A

Cardiac mucosa - mucus secreting glands
Body mucosa - Many gastric pits, parietal cells (eosinophilic) and peptic cells (Haematoxyphilic)
Pyloric mucosa - deeper pits, shorter glands, mostly mucus secreting cells. Fewer parietal cells.

136
Q

Gastric pits

A

Indentations in mucosa lined with foveolar cells. Secrete mucus to protect mucosa from HCl.
Found abundantly in cardiac and pyloric mucosa of stomach.

137
Q

Rugae

A

Longitudinal folds in stomach mucosa. Allow distension of stomach.

138
Q

Epithelium found in the small intestine

A

Simple columnar with microvilli

139
Q

Plicae circularis

A

Circular folds in small intestine wall

140
Q

Peyer’s Patches

A

Small masses of lymphatic tissue found in ileum. Generate antibodies to protect against infection.

141
Q

Sinusoids

A

Small, irregular shaped vessel which receives nutrient rich blood from portal vein and oxygen rich blood from hepatic artery.
Carry blood from edges of lobule to central vein.

142
Q

Kupffer Cell

A

Macrophages found in the liver

143
Q

How does blood plasma move from liver sinusoids to hepatocytes?

A

Endothelial cells have pores and fenestrations.
Basement membrane is discontinuous and non obstructing.
Therefore, plasma can enter Space of Disse (gap between hepatocytes and sinusoid).
Hepatocytes have many microvilli which increase absorption from plasma.

144
Q

Bile is synthesised by…

A

Hepatocytes

145
Q

Canals of Hering

A

Canals into which Bile canaliculi drain bile into after it has been synthesised by hepatocytes.

146
Q

Effect of parasympathetic innervation on salivary secretion

A

Vasodilation - increased blood supply to salivary glands. Watery saliva secreted, containing high HCO3- and Na+ but low K+
(Activates exchange of Cl- for HCO3-, deactivates exchange of Na+ for K+)

147
Q

Effect of sympathetic innervation on salivary secretion

A

Vasoconstriction - reduced blood supply to salivary glands. Dry mouth in response to fear/stress.

148
Q

Function of Intrinsic factor

A

Binds to B12 in duodenum - protecting it from digestion so that it can be absorbed in ileum.

149
Q

Parietal cells in the stomach release…

When stimulated by…

A

Release: Intrinsic Factor and HCl

When stimulated by Gastrin and Histamine

150
Q

Chief Cells in the stomach release…

When stimulated by…

A

Pepsinogen

When stimulated by Gastrin

151
Q

Effects of Gastrin

A

Intrinsic factor and HCl secretion by Parietal cells.

Pepsinogen release by chief cells.

152
Q

D cells in the stomach release…

In response to…

A

Release somatostatin

In response to low pH in stomach (acidity) and secretin

153
Q

Effects of somatostatin

A

Inhibits gastrin release from G cells

154
Q

S cells release…

In response to…

A

Secretin

In response to pH 2-3 in duodenum

155
Q

CCK is released in response to…

A

Products of protein and fat digestion in duodenum.

156
Q

Inhibitors of gastrin secretion

A

CCK
GIP
Somatostatin

157
Q

Deglutition Apnoea

A

Epiglottis covers opening of nasopharynx during swallowing.

Prevents food from entering airway AND inhibits breathing briefly.

158
Q

Mechanism for swallowing

A

Voluntary Phase 1: Tip of tongue pushes against hard palate and contracts.

Involuntary phase 2: Food stimulates mechanoreceptors in pharynx. Contraction of superior constrictor to prevent food entering nasopharynx. Wave of peristaltic contraction propels bolus through upper oesophagus. Relaxation of upper oesophageal sphincter.

Involuntary Phase 3: wave of contraction continues down length of oesophagus (7-10s)

159
Q

Mechanism for HCl secretion from parietal cells

A

Binding of the ligand to cholinergic and gastrin receptors causes activation of PKA and therefore increased Ca2+ (Gq)

Binding of histamine to its receptor causes activation of PKA and therefore increases the effects of gastrin (Gs)

Results in acid secretion

160
Q

Mechanism for inhibition of HCl secretion from parietal cells

A

Somatostatin and prostaglandins bind to their receptors (Gi) causing deactivation of PKA and therefore switching of HCl secretion.

161
Q

Excitatory neurotransmitters in enteric nervous system

A

ACh
Substance P
Neurokinin A

162
Q

Inhibitory neurotransmitters in enteric nervous system

A

NO
ATP
GABA
Neuropeptide Y

163
Q

Composition of saliva

A

Salivary amylase - starch digestion
IgA
Lysozyme
Alkaline fluid

164
Q

How does flow rate affect composition of saliva?

A

Increased flow rate, increases concentration of solutes in saliva (Na+, HCO3- and Cl- BUT NOT K+)
Therefore, increased pH.

165
Q

Phase I of drug metabolism

A

Expose or create a chemically reactive group on the drug to facilitate phase II
e.g. oxidation, de-esterification, reduction or isomerisation

166
Q

Phase II of drug metabolism

A

Deactivate/switch off biochemical or pharmaceutical activity.
Make water soluble by replacing reactive regions with a sugar or sulphate group.

Therefore, prepared for renal/hepatobiliary excretion

167
Q

Cytochrome P450

A

Most significant family in phase I drug metabolism. Oxidative modification of drug molecule.

168
Q

UDP-glucuronyl transferase

A

Phase II drug metabolism.

Conjugates a water soluble Glucuronide to the drug/metabolite (e.g. unconjugated Bilirubin)

169
Q

CYP2E1

A

Metabolism of ethanol

170
Q

CYP1A2

A

Metabolism of caffeine and theophylline

171
Q

CYP1A1

A

Metabolism of theophylline

172
Q

CYP3A4

A

Responsible for half of all phase I metabolism

173
Q

Toxic paracetamol dose

A

4-6g

174
Q

Lethal paracetamol dose

A

> 12g

175
Q

Normal paracetamol dose

A

0.5g

176
Q

Treatment of paracetanol overdose

A

N-Acetyl Cysteine

177
Q

Toxic species generated by phase I metabolism of paracetamol….

How is this removed?

A

N-acetyl P-benzoquinone imine

Deactivated by conjugation to glutathion (phase II metabolism)

178
Q

Metabolism of paracetamol

A

CYP1A2 and CYP2E1 pathway - oxidation of drug which generates NAPBQI. NAPBQI is deactivated by conjugation to glutathione.

UGT pathway - glucuronidation, making it soluble, inactive and easy to excrete.

179
Q

Why does paracetamol overdose cause hepatotoxicity?

A

UGT pathway is overwhelmed. More paracetamol is metabolised via the CYP pathway.
More NAPBQI generated which must be deactivated -
quickly depletes glutathione reserves.
NAPBQI causes significant damage to hepatocytes.

180
Q

Risk factors for dyspepsia

A 
Pregnancy 
Alcohol
Hiatus hernia 
Lactose intolerance 
Peptic or duodenal ulceration 
Stomach cancer
NSAID use 
Anxiety/depression
181
Q

Effect of alcohol on lining of GI tract

A

Alcohol inhibits formation of a protective gel via combination of water with mucins from surface of mucosal cells.

182
Q

Symptoms of dyspepsia

A 
Bloating
Belching 
Retrosternal pain
Epigastric pain/burning 
Nausea 
Reflux (acid taste in mouth)
Heartburn
Fullness/Early satiety
183
Q

What is functional dyspepsia?

A

Most common form of dyspepsia

Delayed gastric emptying - can be caused by diet, stress, H.Pylori

184
Q

Stage I treatment of dyspepsia

A

Antacids - weak bases which react with gastric acid

185
Q

Stage II treatment of dyspepsia

A

H2 Receptor Antagonists - Ranitidine

Competitive inhibition of H2 (histamine) receptors - reduced gastic acid secretion stimulated by histamine (and gastrin)

186
Q

MOA of Ranitidine

A

H2 Receptor Antagonists

Competitive inhibition of H2 (histamine) receptors - reduced gastic acid secretion stimulated by histamine (and gastrin)

187
Q

ADRs of ranitidine

A

Impotence

Gynaecomastia (anti androgen)

188
Q

Stage III treatment of dyspepsia

A

Proton Pump Inhibitors e.g. Omeprazole

Irreversible inhibition of H+K+ATPase

189
Q

MOA of Omeprazole

A

PPI - Irreversible inhibition of H+K+ATPase

190
Q

ADRs of omeprazole

A

Diarrhoea, Nausea, dizziness, headaches, confusion, impotence, gynaecomastia (anti androgen)

191
Q

Causes of gastric ulcers

A

Helicobacter Pylori infection (60%)
NSAIDs (30%)
Carcinoma (5%)
Other (5%)- Crohn’s, neoplasia, stress, 2E syndrome

192
Q

Causes of duodenal ulcers

A

Helicobacter Pylori infection (85%)
NSAIDs (10-14%)
Other (1%)- Crohn’s, neoplasia, stress, 2E syndrome

193
Q

Diagnosis of H.Pylori infection

A

Endoscopy
Urea breath test - 95% sensitive/specific
Stool antigen - 92% sensitive/specific
Serology - 80% sensitive/specific

194
Q

Treatment of H.Pylori infection causing gastric ulceration

A

3, 2, 1 Treatment

3 drugs:
PPI, Amoxicillin + Clarithromycin/Metronidazole

2x per day

For 1 week
(If allergic to penicillin, C+M Abx)

195
Q

HMG CoA Reductase

A

Reduces HMG CoA to Mevalonate which can then be converted to cholesterol

196
Q

St John’s Wart and Oral Contraceptive Pill

A

St John’s Wart induces CYP3A4, increasing the breakdown of the oral contraceptive pill - therefore reducing its efficacy

197
Q

Erythromycin and Oral Contraceptive Pill

A

Erythromycin inhibits CYP3A4, decreasing metabolism of oral contraceptive pill - increased risk of thromboembolic events and other ADRs

198
Q

Fat soluble vitamins

A

ADEK

199
Q

Water soluble vitamins

A

B (B1,2,3,6,9,12) and C

200
Q

Koilonychia

A

Nail spooning - iron deficiency

201
Q

Leukonychia

A

White nails caused by hypoalbuminaemia

202
Q

Dupuytren’s Contracture

A

Contracture of the hand due to palmar fibromatosis - fingers bend towards palm and cannot be fully extended.

Associated with chronic liver disease.

203
Q

Palmar erythema

A

Redness of palms due to chronic liver disease or pregnancy

Anything which causes hyperdynamic circulation

204
Q

Beau’s Lines

A

Deep grooved lines running from side to side on the finger or toenail.

Caused by any illness that interrupts growth of nail bed.

205
Q

Spider naevi

A

Swollen blood vessels slightly beneath the skins surface, often contain a red central spot.

Caused by chronic liver disease, pregnancy or oestrogenic hormones

206
Q

Asterixis Sign

A

Rapid relaxation of dorsiflexion of the wrist - fingers are observed to flap.

Caused by hepatic encephalopathy - imbalance between agonist and antagonist muscle

207
Q

Acanthosis nigricans

A

Darkened, thickened patches of skin in the arm pit.

Associated with carcinoma of stomach and diabetes

208
Q

Causes of abdominal distension

A 
Fat
Flatus
Faeces
Foetus
Fluid
209
Q

Caput Medusae

A

Multiple dilated superficial veins associated with portal hypertension

210
Q

Contraindications for PPIs

A

Osteoporosis

C.Diff infection

211
Q

Risk associated with PPIs and H2 receptor antagonists

A

May mask some symptoms of gastric cancer

212
Q

ADRs of antacids

A

Eructation (burping - due to liberation of CO2 when acid is neutralised)
Diarrhoea

213
Q

Contraindications of antacids

A

Hypophosphataemic
Renal impairment
Hepatic coma (can lead to renal impairment)

214
Q

Why can antacids and PPIs not be given at the same time?

A

PPIs are prodrugs
They rely on the acidity of the stomach to activate them
Neutralisation of stomach acid by antacids will prevent activation of PPI

Year 2 (17 decks)

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