Case 3 Flashcards
(214 cards)
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
2
Q
Negative reinforcement behaviours
A
Relief of bad symptoms - starting to drink alcohol again due to unpleasant withdrawal symptoms
3
Q
Positive reinforcement behaviours
A
Bring about good symptoms - drinking alcohol for euphoric feeling of being intoxicated
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.
5
Q
Dopamine pathway is involved in…
A
Reward, pleasure and euphoria
6
Q
Serotonin pathway is involved in…
A
Mood
Memory
Sleep
Cognition
7
Q
Mallory Weis Syndrome
A
Gastro-oesophageal laceration due to alcoholism, bulimia or any other condition causing violent vomiting.
Causes painful haematemesis.
8
Q
Korsakoff’s Syndrome
A
Persistent amnesia due to chronic alcoholism
9
Q
Transmission of Hep A
A
Faeco oral
10
Q
Risk factors for Hep A
A
Poor sanitation
Gay men
Travellers
11
Q
Prevention of Hep A
A
Vaccination
Hand washing
Food/water hygiene
12
Q
Hepatitis E
A
Very similar to Hep A but very rare.
Associated with animal contact.
13
Q
Treatment for Hep A
A
No specific treatment - spontaneous clearance by immune system.
14
Q
Signs/Symptoms of Hep A
A
Fever
Malaise
Jaundice
15
Q
Transmission of Hep B
A
Blood (assoc with needle stick injury and IV drug use)
Sexual (semen)
Vertical
16
Q
Acute Hep B can become chronic, what is the chance of HBV becoming chronic?
A
95% in neonates
<5% in adults
17
Q
Definition of chronic HBV
A
Failure to clear after 6 months
18
Q
Effects of chronic HBV
A
End stage liver disease - portal hypertension/ascites, bleeding oesophageal varices, liver failure
19
Q
Vaccination is available for which forms of hepatitis
A
A and B
20
Q
Transmission of Hep C
A
Blood and vertical
21
Q
Acute Hep C can become chronic. What is the chance of Hep C becoming chronic?
A
85% (15% will recover)
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
23
Q
Hepatitis D
A
Only presents WITH Hep B
Very high incidence of cirrhosis development
24
Q
Features of liver cirrhosis
A
Ascites and oedema Impaired immunity Oesophageal Varices Splenomegaly Testicular atrophy Gynaecomastia Spider Naevi
25
Why does liver cirrhosis cause oedema?
Low albumin
| Increased hydrostatic pressure of blood
26
Why does liver cirrhosis cause ascites?
Low albumin
| Portal hypertension
27
Why does liver cirrhosis cause oesophageal varices and splenomegaly?
Portal hypertension
28
Why does liver cirrhosis cause Testicular atrophy and Gynaecomastia
Impaired metabolism of oestrogen
29
HBcAg
Core antigen
| Present during acute infection
30
HBsAg
Surface antigen
| Present during active infection
31
HBsAb
Surface antibody
| Present in an immune person
32
HBcAb
Core antibody
Present in someone who has had the infection in the past.
Does not provide immunity
33
How is vertical transmission of HBV prevented?
Antiviral therapy to mother during pregnancy.
Passive immunisation of mother (eAg)
Vaccination of infant (3 dose schedule, started at birth)
34
Oesophageal varices
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
35
Symptoms of GORD
Heartburn
Dysphagia
Sour taste in mouth
36
Causes of GORD
Dysfunction of lower oesophageal sphincter
Hiatus Hernia
Delayed gastric emptying (functional dyspepsia)
37
Sliding hiatus hernia
Diaphragm no longer supporting lower oesophageal sphincter.
| Upper part of stomach can slide through.
38
Rolling hiatus hernia
Part of stomach herniates into chest next to normal oesophagus.
Looks like a balloon next to oesophagus.
39
Barrett's Oesophagus
Metaplasia of lower oesophageal squamous epithelium to gastric columnar due to chronic acid exposure.
Can lead to adenocarcinoma
40
How is cholesterol converted to bile salts?
Cholesterol converted to bile acids by Cytochrome P450.
| Bile acids are conjugated to glycine or taurine by liver cells to form bile salts.
41
Primary vs secondary bile salts
Primary - formed by hepatocytes
| Secondary - formed by bacteria in the intestine
42
How are bile salts recycled?
Absorbed in GI tract and enter portal circulation.
| Active reuptake of bile salts from blood into liver cells via sodium dependent transporters
43
HMG CoA Reductase
Enzyme responsible for cholesterol synthesis.
| Inhibited by statins.
44
Bilirubin Metabolism
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.
45
Conjugation of bilirubin
UDP-glucuronic acid supplies glucuronic acid, leaving UDP remaining.
Bilirubin also loses albumin
46
Signs/Symptoms of jaundice
Dark urine - excretion of bilirubin via kidneys
Pale stools with fatty streaks (absence of bilirubin and poor fat digestion)
Itching (accumulation of bile acids)
47
Conjugated bilirubin converted to urobilinogen by...
Bacterial flora of the colon.
48
Function of LDL
Carries cholesterol from liver to tissues
49
Function of HDL
Carries cholesterol from tissues to liver
50
Length of thoracic oesophagus
23cm
51
Length of abdominal oesophagus
2cm
52
Muscle distribution in oesophagus
Superior 1/3 = Voluntary striated
Middle 1/3 = mixture
Inferior 1/3 = smooth muscle
53
Vertebral level of oesophageal hiatus
T10
54
Greater curvature of stomach is supplied by
Short gastric arteries
| Right and left omental arteries
55
Lesser curvature of the stomach is supplied by
Left gastric artery
| Right gastric branch of hepatic artery
56
Epiploic foramen
Allows communication between greater and lesser sac
57
Lesser omentum
Connects stomach to duodenum and liver
58
Function of Greater omentum
Involved in combating GI infection - contains many lymph nodes with macrophages
59
Parasympathetic innervation of stomach
Vagus nerve
Increased stomach motility, gastric juice secretion and relaxation of sphincter
60
Sympathetic innervation of stomach
Coeliac plexus
Reduced stomach motility and gastric juice secretion. Constriction of sphincters
61
Transition from foregut to midgut occurs at...
Major Duodenal Papilla in superior duodenum
62
Distinguishing features of jejunum
Red
Thick walled
Long vasa recta (straight arteries)
Less arcades (arterial loops)
63
Distinguishing features of ileum
Pink
Thin walled
Short vasa recta
More arcades
64
Primary site of lipid absorption
Jejunum
65
Primary site of bile salt absorption
Ileum
66
Primary site of cobalamin (Vit B12) absorption
Ileum
67
LFTs: Elevated ALP - Alkaline Phosphatase
When bile flow is obstructed or biliary tree is damaged
| When canaliculi or hepatocytes are damaged
68
LFTs Elevated AST - Aspartate Transaminase
When hepatocellular necrosis occurs BUT also in heart, muscle, kidney and brain injury
69
LFTs: Elevated ALT
A more specific measure than AST. Only increased with liver failure
70
LFTs: Low albumin indicates...
Chronic liver disease - reduced synthetic capability of liver.
OR
Inflammation - redistribution of albumin into extracellular space of plasma compartment
71
LFTs: Prothombin time
More sensitive indicator than albumin since clotting factors have a shorter half life.
Elevated PT in chronic liver dysfunction
72
Causes of prehepatic unconjugated hyperbilirubinaemia
```
Haemolytic anaemia
Defects in RBC membranes
Defects in Hb production
Sickle cell anaemia
Defect in RBC metabolism
```
73
Mechanism for prehepatic unconjugated hyperbilirubinaemia
Bilirubin is produced at a greater rate than the capacity of the liver to conjugate it.
i.e. excessive breakdown of RBCs
74
Lab results for prehepatic unconjugated hyperbilirubinaemia
```
Raised plasma unconjugated bilirubin.
Normal conjugated bilirubin (since liver is functioning normally)
Raised reticulocytes (immature RBCs)
Low Hb
Normal LFTs
```
75
Mechanism for Hepatic unconjugated hyperbilirubinaemia
Reduced conjugated and excretion of bilirubin
76
Causes of Hepatic unconjugated hyperbilirubinaemia
Crigler Najjar Syndrome - lack of conjugating enzyme
Gilbert's - mild deficiency of conjugating enzyme
Newborns with immature liver.
77
Lab results for hepatic unconjugated hyperbilirubinaemia
Raised plasma unconjugated bilirubin
No urinary conjugated bilirubin
Raised AST, ALP and GGT
78
LFTs: Gamma-Glutamyl Transferase
Found almost exclusively in the liver
| Increased during cholestasis or hepatocellular disease
79
Mechanism for hepatic conjugated hyperbilirubinaemia
Liver damage leading to reduced uptake of unconjugated bilirubin from plasma
80
Causes of hepatic conjugated hyperbilirubinaemia
Viral or toxic hepatitis or cirrhosis causing leakage of bilirubin from hepatocytes.
Dubin-Johnson Disease (deficiency in conjugated bilirubin transport into canaliculi)
81
Lab results in hepatic conjugated hyperbilirubinaemia
Raised plasma conjugated bilirubin (leaking out of hepatocytes)
Raised urine conjugated bilirubin and urobilinogen
Raised ALT and AST
82
Causes of post-hepatic conjugated hyperbilirubinaemia
```
Gall stones
Biliary stricture
Cancer
Biliary cirrhosis
Drugs
Acute hepatocellular damage e.g. infection
```
83
Lab results for post-hepatic conjugated hyperbilirubinaemia
Elevated plasma and urine conjugated bilirubin
No urobilinogen (since bilirubin cannot leave liver)
Raised ALP, AST, ALT and GGT
84
Cholesterol based gall stones
80% of cases
Occur when bile contains too much cholesterol and too little bile salts
Less calcium
Green/Brown in colour
85
Pigment gall stones
20% of cases
Composed of bilirubin pigment and calcium salts.
Small and dark
86
Risk factors for cholesterol gall stones
Increased cholesterol - female, increased age, obesity
Increased bile salts - high oestrogen, malabsorption
87
Risk factors for pigment gall stones
Increased RBC breakdown (e.g. sickle cell anaemia) - causing increased unconjugated bilirubin.
Chronic biliary infected - causing glucuronidase production by epithelium or bacteria.
88
Hartmann's Pouch
Mucosal fold at neck of gallbladder
| Common site for gallstones to become lodged.
89
Symptoms of gallstone lodged in common hepatic bile duct
Post-hepatic Conjugate Hyperbilirubinaemia
| Dark urine, pale stools, yellow skin, fatty streaks in stool.
90
Symptoms of gallstone lodged in Ampulla of Vater
Post-hepatic Conjugate Hyperbilirubinaemia
Dark urine, pale stools, yellow skin, fatty streaks in stool
Plus pain in abdomen and back due to pancreatitis.
91
Acute Pancreatitis
Blockage of duct causing injury to acini cells since activated digestive enzymes are trapped in pancreas.
92
Symptoms of Chronic Pancreatitis
Steatorrhoea
| Flatulence and fowl smelling stools (inability to digest proteins, bacterial growth in intestines)
93
Acinar cells of pancreas release...
In response to...
```
Pancreatic enzymes (protease, amylase and lipase)
Cl- rich secretions
```
In response to CCK
94
Ductal cells of acini of pancreas release...
In response to...
HCO3- (exchanged for Cl- released by acinar cells)
In response to secretin and ACh
95
How does Secretin bring about alkaline secretions from pancreatic acinus?
```
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
CFTR Channel
Cystic Fibrosis Transmembrane Conductance Regulator (encoded by CFTR gene)
Transport of Cl- across apical membrane of acini.
Regulated by cAMP
Ca2+ dependent.
97
Hormonal and neural control mechanisms involved in CEPHALIC phase of digestion
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
Hormonal and neural control mechanisms involved in GASTRIC phase of digestion
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
Hormonal and neural control mechanisms involved in INTESTINAL phase of digestion
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
Proteolytic component of pancreatic secretions
Trypsin, chymotrypsin and elastase (endopeptidases)
| Carboxypeptidases (attack terminal bond)
101
Liplytic component of pancreatic secretions
Colipase, cholesterol esterase and PLA2 secreted as zymogens.
102
What is the significance of trypsin in exocrine pancreatic secretions?
Activates zymogen granules of all proteolytic and lipolytic pancreatic secretions.
Activated by enteropeptidase.
103
Cholagogue
Promotes discharge of bile
104
Orexin is released from...
In response to ...
Released from lateral and posterior hypothalamus
In response to low blood glucose and high ghrelin.
105
Ghrelin is released from...
In response to...
Released from gastric mucosa of stomach and small intestine.
In response to empty stomach, hypoglycaemia
106
Leptin is released from...
In response to...
Released from adipocytes
In response to distension of stomach and presence of glucocorticoids (insulin)
107
Leptin is responsible for...
Suppression of appetite
Brown fat metabolism
Maintenance of baseline weight
108
CCK is released from...
In response to...
released from I cells in duodenal mucosa.
In response to products of protein and fat digestion in duodenum
109
CCK is responsible for...
Suppression of appetite
Slowing of gastric emptying
Contraction of gallbladder
110
PYY is released from...
In response to...
Released from L cells in colon and ileum.
In response to calorie intake
111
PYY is responsible for..
Suppression of appetite
| Slowing of peristalsis to maximise absorption.
112
Cause of fatty change in the liver
| White droplets
Metabolic stress
Alcohol
Pregnancy
113
Liver change which occurs as a result of cholestatic obstruction
Proliferation of bile ducts
Also occurs as a result of autoimmune disease, viral hepatitis, pregnancy and some drugs.
114
Hepatocyte necrosis
Affects individual cells, usually in zone 3 of liver acini (poorer blood supply)
Cells have a shrunken nucleus
115
How does liver fibrosis differ from cirrhosis?
Fibrosis results from inflammation and is reversible.
| Cirrhosis results from repetitive injury and is irreversible.
116
Why is liver at a high risk of metastatic cancer?
Dual blood supply
117
Drugs which can cause dose-dependent liver damage
Paracetamol (in over dose) - zone 3 necrosis
| Methotrexate - fibrosis
118
Glisson's Capsule
Fibrous layer coating the liver
119
Falciform ligament
Attaches anterior surface of liver to anterior abdominal wall
Free edge contains ligamentum teres (remnant of umbilical vein)
120
Lobes of the liver
Left
Right
Quadrate (anterior)
Caudate (posterior)
121
Morrison's Pouch
Hepatorenal recess - most likely place for fluid collection in a bed-ridden px
122
Blood supply to the liver:
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
Autonomic nerve supply to liver
Parasympathetic - vagus nerve
| Sympathetic - coeliac plexus
124
Sphincter of Oddi
Opening of hepatopancreatic Ampulla of Vater into duodenum.
125
Vasculature of gallbladder
Arterial supply - cystic artery (branch of common hepatic)
Venous drainage - cystic vein (drains into portal vein)
126
Autonomic innervation of gallbladder
Sympathetic - coeliac plexus
| Parasympathetic - vagus nerve
127
Epithelium which lines the gall bladder
Simple columnar
128
Connective tissue on the outer surface of the gallbladder
Adventitia - where GB attaches to liver
| Serosa - at free edge
129
Serosa
Encloses body cavities. Consists of a thin layer of connective tissue and a layer of cells secreting serous fluid.
130
Adventitia
Thin layer of connective tissue
131
Function of myenteric plexus
Motor innervation of GI tract.
132
Function of submucosal plexus
Carries sensory information from stretch receptors
| Regulates secretory activity of the GI tract.
133
Effects of perforation of oesophagus
Contents extravasates into mediastinum.
| Causes breathing difficulties and lung infection.
134
Epithelium found in the stomach
Simple columnar
135
Distribution of mucosa in the stomach
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
Gastric pits
Indentations in mucosa lined with foveolar cells. Secrete mucus to protect mucosa from HCl.
Found abundantly in cardiac and pyloric mucosa of stomach.
137
Rugae
Longitudinal folds in stomach mucosa. Allow distension of stomach.
138
Epithelium found in the small intestine
Simple columnar with microvilli
139
Plicae circularis
Circular folds in small intestine wall
140
Peyer's Patches
Small masses of lymphatic tissue found in ileum. Generate antibodies to protect against infection.
141
Sinusoids
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
Kupffer Cell
Macrophages found in the liver
143
How does blood plasma move from liver sinusoids to hepatocytes?
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
Bile is synthesised by...
Hepatocytes
145
Canals of Hering
Canals into which Bile canaliculi drain bile into after it has been synthesised by hepatocytes.
146
Effect of parasympathetic innervation on salivary secretion
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
Effect of sympathetic innervation on salivary secretion
Vasoconstriction - reduced blood supply to salivary glands. Dry mouth in response to fear/stress.
148
Function of Intrinsic factor
Binds to B12 in duodenum - protecting it from digestion so that it can be absorbed in ileum.
149
Parietal cells in the stomach release...
When stimulated by...
Release: Intrinsic Factor and HCl
When stimulated by Gastrin and Histamine
150
Chief Cells in the stomach release...
When stimulated by...
Pepsinogen
When stimulated by Gastrin
151
Effects of Gastrin
Intrinsic factor and HCl secretion by Parietal cells.
| Pepsinogen release by chief cells.
152
D cells in the stomach release...
In response to...
Release somatostatin
In response to low pH in stomach (acidity) and secretin
153
Effects of somatostatin
Inhibits gastrin release from G cells
154
S cells release...
In response to...
Secretin
In response to pH 2-3 in duodenum
155
CCK is released in response to...
Products of protein and fat digestion in duodenum.
156
Inhibitors of gastrin secretion
CCK
GIP
Somatostatin
157
Deglutition Apnoea
Epiglottis covers opening of nasopharynx during swallowing.
| Prevents food from entering airway AND inhibits breathing briefly.
158
Mechanism for swallowing
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
Mechanism for HCl secretion from parietal cells
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
Mechanism for inhibition of HCl secretion from parietal cells
Somatostatin and prostaglandins bind to their receptors (Gi) causing deactivation of PKA and therefore switching of HCl secretion.
161
Excitatory neurotransmitters in enteric nervous system
ACh
Substance P
Neurokinin A
162
Inhibitory neurotransmitters in enteric nervous system
NO
ATP
GABA
Neuropeptide Y
163
Composition of saliva
Salivary amylase - starch digestion
IgA
Lysozyme
Alkaline fluid
164
How does flow rate affect composition of saliva?
Increased flow rate, increases concentration of solutes in saliva (Na+, HCO3- and Cl- BUT NOT K+)
Therefore, increased pH.
165
Phase I of drug metabolism
Expose or create a chemically reactive group on the drug to facilitate phase II
e.g. oxidation, de-esterification, reduction or isomerisation
166
Phase II of drug metabolism
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
Cytochrome P450
Most significant family in phase I drug metabolism. Oxidative modification of drug molecule.
168
UDP-glucuronyl transferase
Phase II drug metabolism.
| Conjugates a water soluble Glucuronide to the drug/metabolite (e.g. unconjugated Bilirubin)
169
CYP2E1
Metabolism of ethanol
170
CYP1A2
Metabolism of caffeine and theophylline
171
CYP1A1
Metabolism of theophylline
172
CYP3A4
Responsible for half of all phase I metabolism
173
Toxic paracetamol dose
4-6g
174
Lethal paracetamol dose
>12g
175
Normal paracetamol dose
0.5g
176
Treatment of paracetanol overdose
N-Acetyl Cysteine
177
Toxic species generated by phase I metabolism of paracetamol....
How is this removed?
N-acetyl P-benzoquinone imine
Deactivated by conjugation to glutathion (phase II metabolism)
178
Metabolism of paracetamol
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
Why does paracetamol overdose cause hepatotoxicity?
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
Risk factors for dyspepsia
```
Pregnancy
Alcohol
Hiatus hernia
Lactose intolerance
Peptic or duodenal ulceration
Stomach cancer
NSAID use
Anxiety/depression
```
181
Effect of alcohol on lining of GI tract
Alcohol inhibits formation of a protective gel via combination of water with mucins from surface of mucosal cells.
182
Symptoms of dyspepsia
```
Bloating
Belching
Retrosternal pain
Epigastric pain/burning
Nausea
Reflux (acid taste in mouth)
Heartburn
Fullness/Early satiety
```
183
What is functional dyspepsia?
Most common form of dyspepsia
| Delayed gastric emptying - can be caused by diet, stress, H.Pylori
184
Stage I treatment of dyspepsia
Antacids - weak bases which react with gastric acid
185
Stage II treatment of dyspepsia
H2 Receptor Antagonists - Ranitidine
Competitive inhibition of H2 (histamine) receptors - reduced gastic acid secretion stimulated by histamine (and gastrin)
186
MOA of Ranitidine
H2 Receptor Antagonists
Competitive inhibition of H2 (histamine) receptors - reduced gastic acid secretion stimulated by histamine (and gastrin)
187
ADRs of ranitidine
Impotence
| Gynaecomastia (anti androgen)
188
Stage III treatment of dyspepsia
Proton Pump Inhibitors e.g. Omeprazole
Irreversible inhibition of H+K+ATPase
189
MOA of Omeprazole
PPI - Irreversible inhibition of H+K+ATPase
190
ADRs of omeprazole
Diarrhoea, Nausea, dizziness, headaches, confusion, impotence, gynaecomastia (anti androgen)
191
Causes of gastric ulcers
Helicobacter Pylori infection (60%)
NSAIDs (30%)
Carcinoma (5%)
Other (5%)- Crohn's, neoplasia, stress, 2E syndrome
192
Causes of duodenal ulcers
Helicobacter Pylori infection (85%)
NSAIDs (10-14%)
Other (1%)- Crohn's, neoplasia, stress, 2E syndrome
193
Diagnosis of H.Pylori infection
Endoscopy
Urea breath test - 95% sensitive/specific
Stool antigen - 92% sensitive/specific
Serology - 80% sensitive/specific
194
Treatment of H.Pylori infection causing gastric ulceration
3, 2, 1 Treatment
3 drugs:
PPI, Amoxicillin + Clarithromycin/Metronidazole
2x per day
For 1 week
(If allergic to penicillin, C+M Abx)
195
HMG CoA Reductase
Reduces HMG CoA to Mevalonate which can then be converted to cholesterol
196
St John's Wart and Oral Contraceptive Pill
St John's Wart induces CYP3A4, increasing the breakdown of the oral contraceptive pill - therefore reducing its efficacy
197
Erythromycin and Oral Contraceptive Pill
Erythromycin inhibits CYP3A4, decreasing metabolism of oral contraceptive pill - increased risk of thromboembolic events and other ADRs
198
Fat soluble vitamins
ADEK
199
Water soluble vitamins
B (B1,2,3,6,9,12) and C
200
Koilonychia
Nail spooning - iron deficiency
201
Leukonychia
White nails caused by hypoalbuminaemia
202
Dupuytren's Contracture
Contracture of the hand due to palmar fibromatosis - fingers bend towards palm and cannot be fully extended.
Associated with chronic liver disease.
203
Palmar erythema
Redness of palms due to chronic liver disease or pregnancy
| Anything which causes hyperdynamic circulation
204
Beau's Lines
Deep grooved lines running from side to side on the finger or toenail.
Caused by any illness that interrupts growth of nail bed.
205
Spider naevi
Swollen blood vessels slightly beneath the skins surface, often contain a red central spot.
Caused by chronic liver disease, pregnancy or oestrogenic hormones
206
Asterixis Sign
Rapid relaxation of dorsiflexion of the wrist - fingers are observed to flap.
Caused by hepatic encephalopathy - imbalance between agonist and antagonist muscle
207
Acanthosis nigricans
Darkened, thickened patches of skin in the arm pit.
Associated with carcinoma of stomach and diabetes
208
Causes of abdominal distension
```
Fat
Flatus
Faeces
Foetus
Fluid
```
209
Caput Medusae
Multiple dilated superficial veins associated with portal hypertension
210
Contraindications for PPIs
Osteoporosis
| C.Diff infection
211
Risk associated with PPIs and H2 receptor antagonists
May mask some symptoms of gastric cancer
212
ADRs of antacids
Eructation (burping - due to liberation of CO2 when acid is neutralised)
Diarrhoea
213
Contraindications of antacids
Hypophosphataemic
Renal impairment
Hepatic coma (can lead to renal impairment)
214
Why can antacids and PPIs not be given at the same time?
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
