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Sem 2 year 2 > The Patient > Flashcards

The Patient Flashcards

1
Q

How long is the small intestine?

A

20 feet

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2
Q

Which enzymes are secreted from the salivary glands?

A

Amylase

Lipase

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3
Q

What are the three types of salivary galnds?

A

Sublingual
Submandibular
Parotid

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4
Q

Which gland does mups affect?

A

Parotid

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5
Q

Which nerves are involved in the process of swallowing?

A

Trigeminal, facial, glossopharyngeal, hypoglossal and vagus

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6
Q

What is hiatus hernia?

A

Part of stomach moves up into chest and is associated with hiatus hernia

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7
Q

What are people with Barrett’s oesophagus more at risk of?

A

Adenocarcinoma - a type of cancer

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8
Q

What are the gastric cell types?

A

Mucous cells
G-cells
Chief cells
Parietal cells

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9
Q

Which drugs can reduce acid reflux?

A

H2 receptor agonists

PPI’s

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10
Q

How do H2 receptor agonists work?

A

Block histamine receptors to reduce acid production

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11
Q

How do PPI’s work?

A

Irreversibly bind to the -SH groups and block protein function

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12
Q

What is the ailmentary canal?

A

The whole passage along which food passes through the body from mouth to anus during digestion

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13
Q

Why is insulin hard to deliver?

A

Pepsin is a protease that hydrolyses it

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14
Q

Examples of drugs absorbed in the stomach

A

Aspirin, paracetamol, warfarin

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15
Q

What prevents self digestion?

A

Pepsin released as Pepsinogen (zymogen) which is inactive of surface of cell tissues

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16
Q

Why does the HCl secreted by the stomach not cause 1st and 2nd degree burns?

A

Mucus secreted by foveolar cells
Tight juctions
High cell turnover

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17
Q

What affects does mucus have?

A

Neutralises HCl
Moves along mucosa
Forms a physical barrier preventing exposure

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18
Q

What affect do tight junctions have?

A

Protein complexes lock epithelial cells

Restricts movement of acid/protease between cells down to underlaying tissue

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19
Q

What affect does a high cell turnover have?

A

Every 2-3 days damaged cells replaced - cells from gastric pits

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20
Q

What would happen if there is a breakdown in mucus barrier function?

A

Epithelial cells exposed to HCl and pepsin
Gastric/duodenal ulcer which may extend and damage blood vessels and cause haemorrhage
Severe cases - complete erosion through tract wall called perforated ulcer which can lead to peritonitis

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21
Q

What does Helicobacter pylori do?

A

Infects gastric mucosa

Decreases barrier efficacy so ulcer caused

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22
Q

How do you treat H.pylori?

A

2 x antibiotics + PPI

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23
Q

What is peristalsis?

A

The wave of muscular contraction along GI tract

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24
Q

What is the process of peristalsis?

A

Circular muscles contract behind
Longitudinal muscles contract to push along
Then the same thing happens again

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25
Q

What happens during diarrhoea?

A

Reduced longitudinal smooth muscle activity so retain contents of the intestine longer so exposed to epithlium to increased water absorption

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26
Q

What controls muscle contractions during peristalsis?

A

A neurone in the Myenteric plexus

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27
Q

How does loperamide work to stop diarrhoea?

A

Binds to µ opiod receptors of the MP and reduced contraction of the muscles

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28
Q

What are the side effects of opioid pain relief?

A

Constipation

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29
Q

Why are bile acids important?

A

When released into the intestine the emulsify lipids to lead to absorption
Vitamins A,D,E,K are absorbed this way

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30
Q

Where are bile acids stored?

A

In the liver

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31
Q

Where do the bile acids move?

A

Bile duct
duodenum
Ileum
Back into the liver

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32
Q

What is dyspepsia?

A

Persistent or recurrent pain or discomfort in upper abdomen

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33
Q

What are the causes of dyspepsia?

A

Lifestyle factors
Medication
Diseases

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34
Q

What is GORD and what causes it?

A

Symptoms/complications resulting from reflux gastric contents into oesophagus, oral cavity or lung due to lower oesophageal sphincter relaxation

Obesity 
Genetic
Lifestyle
Medication 
Age
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35
Q

What are peptic ulcers and what are the two types?

A

Open sores that develop on the inside lining of the oesophagus, stomach or upper portion small intestine
>5mm diameter with associated inflammation
Imbalance in agents that protect the epithelium and those which attack
Gastric or duodenal

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36
Q

What are the symptoms of a peptic ulcer?

A 
Upper abdominal pain, tenderness, discomfort 
Heartburn/reflux 
Bloating 
Early satiety
Nausea and vomiting
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37
Q

What are the symptoms of a GASTRIC peptic ulcer?

A

Pain radiates to back
Mainly occurs at night
Aggravated by food
Lose weight

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38
Q

What are the symptoms of a DUODENAL peptic ulcer?

A

Epigastric pain
Anytime – empty stomach
Relieved by food/antacids
Gain weight

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39
Q

What are the alarm signs for PUC

A 
Anemia
Weight loss
Anorexia
Recurrent problems (>55)
Melaena/haematemesis
Swallowing problems
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40
Q

How do antacids work and when are they used?

A

Neutralise acids

Use when requires, between meals and bedtimes, 4+ times daily

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41
Q

What are the side effects of antacids?

A

Mg - laxative effects
Al - constipation effecr
Ca - possible rebound acid secretion/hypercalcaemia

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42
Q

What is low sodium content in an antacid classed as?

A

less than 1 mmol

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43
Q

If an antacid interacts with other meds, what may happen?

A

Impaired absorption of other drugs
Raises pH so may damage enteric coatings
May affect pH dependent renal excretion

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44
Q

How do alginates work?

A

Increase viscosity of stomach contents

Form a raft that floats on top of stomach contents and protects mucosa

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45
Q

How do Histamine H2 receptor antagonists work?

A

Reduce gastric acid output by blocking histamine H2 receptor bloackade

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46
Q

What are Histamine H2 receptor antagonists licensed for?

A 
GORD
Maitainance treatment
NSAID prophylaxis
Functional dyspepsia
Stress ulcer prophylaxis
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47
Q

Give Histamine H2 receptor antagonists examples

A

Ranitidine
Cimetidine
Famotidine

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48
Q

What interactions does Cimetidine have

A

Warfarin
Phenytoin, carbamazepine, valproate
Theophylline
Sildenafil

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49
Q

How do PPI’s work?

A

Block gastric H,K-ATPase, inhibiting gastric acid secretion

(final pathway in gastric acid production)

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50
Q

Give examples of PPI’s

A 
Esomeprazole
Lansoprazole
Omeprazole
Pantoprazole
Rabeprazole
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51
Q

How many times a day do you take PPI’s

A

Once or twice generally

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52
Q

What are the indications for PPI’s?

A

Dyspepsia
GORD
Treatment of gastric and duodenal ulcers
Maintenance treatment
NSAID prophylaxis
Excessive gastric acid secretion
stress ulcer prophylaxis, peri-operatively

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53
Q

Long term PPI therapy is associated with the risk of adverse effects - what do these include?

A 
Gastric cancer
H Pylori infection 
Pneumonia
C diff infection
Bacterial overgrowth, reduced calcium absorption leading the hip fracture
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54
Q

What do PPI’s interact with?

A

Antireterovirals
Methotrexate
Citalopram
Omeprazole reduces efficacy of Clopidogrel

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55
Q

What does H Pylori cause?

A

Gastritis

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56
Q

How do we test for H Pylori

A

Antibodies
Urea breath test
Stool antigen test
Mucosal biopsies

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57
Q

Why do we need to take a careful drug history when testing for H Pylori?

A

Some drugs can give false positives or false negatives

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58
Q

What is the treatment for H Pylori?

A

2 day, BD course of PPI plus 2 antibiotics

1st line - PPI full dose BD, Amoxicillin 1g BD, Clarithromycin 500mg BD or Metronidazole 400mg BD

If penicillin allergy, just PPI+Clarithromycin 500mg BD and Metronidazole 400mg BD

If penicillin allergic and previous clarithromycin exposure/treatment failure - PPI+ combination of two or more bacterials (bisulth, tetracycline, quinolone, metronidazole, clarithromycin)

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59
Q

When treating H Pylori, what interactions should you warn the patient about?

A

Clarithromycin and statins

Metronidazole and alcohol

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60
Q

What are the risk factors for an NSAID bleed?

A 
Age > 60
Multiple NSAIDs 
Smoker 
H pylori infection 
Concurrent medication including steroids, anticoagulants 
Higher dose/longer duration
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61
Q

What is the mechanism for NSAID induced ulcers?

A

Inhibition of prostaglandin synthesis impairs mucosal defences so there is an erosive breach of the epithelial barrier

Acid attack deepens into frank ulceration

Low pH encourages passive absorption of NSAID so trapped in mucosa

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62
Q

What are the indirect mechanisms of NSAID damage?

A

Reduced gastric blood flow
Reduced mucus and bicarbonate production
Leads to decreased cell repair

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63
Q

What is done to manage NSAID induced PUD?

A

Stop NSAID id possible
Test for H Pylori
Treat with full dose PPI or H2 receptor antagonist for 8 weeks
If H Pylori present give eradication therapy AFTER
If they need to stay on the NSAID, give gastroprotection - low dose PPI, H2 receptor antagonist, Misoprostol

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64
Q

Misoprostol
Use
Side effects
Contraindications

A

It is a prostaglandin analogue
Preventing NSAID induced PUD
SE - diarrhoea
c/i - pregnancy as its a uterine stimulant

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65
Q

Why is dyspepsia and GORD more likely in pregnancy?

A

Less sphincter tone so more likely to get reflux

Mechanical and hormonal factors

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66
Q

Why is GORD and reflux common in children and when does it resolve?

A

GIT is still developing

Usually resolves by 12-18 months

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67
Q

How can you manage GORD and reflux in children?

A 
Change frequency and volume of feed
Feed thickener or thickened formula feed
Use alginate instead of thickened feeds
H2 receptor antagonist
PPI
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68
Q

How is GORD and dyspepsia in pregnancy managed?

A

Dietary and lifestyle changes
Antacid or alginate (but avoid sodium bicarbonate or magnesium trisilicate)
If symptoms severe or persist give Ranitidine or Omeprazole

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69
Q

What can the small intestines surface are be compared to?

A

A tennis court

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70
Q

What adaptions does the small intestine have?

A

Pilcae
Epithlium
Enzymes

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71
Q

Describe the pilcae on small intestine

A

Folds
Covered with finger like projections called villi (1mm high)
Villi lined with epithelial cells that have microvilli

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72
Q

Describe the small intestine epithelium

A

1 cell thick

So minimal barrier to transfer of molecules from lumen

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73
Q

What do the enzymes in the small intestine do?

A

Convert non-absorbable macromolecules to absorbable small molecules

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74
Q

What are the products of sucrose, lactose and maltose digestion?

A

sucrose -Glucose and fructose
Lactose - glucose and galactose
maltose - glucose and glucose

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75
Q

How does glucose cross the epithelium?

A

SGLT1 Transporter in basolateral membrane
Glucose binds to glucose transporter
High conc of sodium ions outside too -Sodium ions bind to transporter
Transporter has a conformational change and flips to face inside the cell
Glucose and sodium ions move into the cell

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76
Q

How does fructose cross the epithelium?

A

GLUT5 transporter in basolateral membrane

Also sodium dependent

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77
Q

How do proteins cross the epithelium wall?

A

Digested to smaller peptides then to AA
Small peptides - PEPT1 transporter
H+ dependent

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78
Q

What aspect of drug transport do drug designers exploit?

A

Drug UPTAKE transporters are very efficient

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79
Q

Give examples of drugs that are PEPT1 Substrates

A 
Cephalosporins
Penicillins
Enalapril
α-Methlydopa-phenylalanine
Val-acyclovir
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80
Q

Give examples of drugs which are OCTN2 substrates

A 
quinidine
verapamil
imatinib
Valproic acid
α-Methlydopa-phenylalanine
Val-acyclovir
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81
Q

Give examples of drugs which are OATP2B1 substrates

A

Pravastatin
Rosuvastatin
Atorvastatin
Fexofenadine

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82
Q

What do drug efflux transporters do?

A

Eject compounds from the cell - drugs enter enterocytes and are actively effluxed into the gut lumen
Uses ATP
Can be detrimental to drug absorption

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83
Q

Give examples are efflux transporters

A

P-gp

BCRP

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84
Q

Give examples of P-gp substrates

A

HIV PI
Immunosuppressants
Antibiotics
Cardiotonics (digoxin, quinidine)

Verapamil, Quinidine, Imatinib are OCTN2 substrates so there is a competition between uptake and efflux

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85
Q

What is extravasation and what does it cause?

A

Drug leaks onto surrounding tissue and causes necrosis (conc drug)

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86
Q

In a study, oral anti cancer drugs and a P-gp modulator were given, what was the outcome? Which drugs were used?

A

All increased toxicity

Etoposide
Doxorubicin
Paclitaxel

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87
Q

Digoxin has a narrow therapeutic window - which clinical P-gp interactions can occur? What affect does this have?

A

Ritonavir
Atorvastatin
Talinolol

Increase in digoxin AUC and side effects

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88
Q

What are the two blood supplies to the liver?

A 
Arterial blood (20% hepatic artery)
Venous blood (80% portal vein
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89
Q

What are the functions of the liver?

A 
Metabolism
Synthesis
Immunological
Storage
Homeostasis
Production of bile
Clearance

Need to learn the substrates of these

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90
Q

What are the main patterns of liver damage and what do they lead to?

A

Cholestatic
Hepatocellular
Leas to fibrosis and cirrhosis

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91
Q

What is cholestasis? What are the two types? What does it cause?

A

Bile sites in bile ducts and causes damage
Intrahepatic - bilary ductules
Extrahepatic - mechanical obstruction
Increase in liver enzymes
Impaired biliary excretion and reduced absorption of fatty substances
Accumulation - damage of hepatocytes - jaundice and itching

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92
Q

What is Hepatocellular disease? What are the two types? What does it cause?

A 
Injury to hepatocytes by toxins or viruses
Fatty infiltration - steatosis
Inflammation - Hepatitis
Necrosis if it persists
Increase in liver enzymes
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93
Q

What is fibrosis and how does it lead to cirrhosis?

A

Persistent, extensive hepatocyte damage -active formation and deposition of collagen formation of scar tissue (fibrosis)
Disruption of blood flow and more scar tissue
Erratic regeneration nodules can form
Lead to cirrhosis (extensive damage)

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94
Q

What affect does alcohol have on the liver?

A

Stenosis and hepatitis (cells change shape, fat deposits and inflammation)
Cirrhosis - blood doesn’t flow through well

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95
Q

What is the usual range of Bilirubin?

A

5-20mmol/L

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96
Q

What is bilirubin a product of?

A

RBC breakdown

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97
Q

What do higher levels of bilirubin increase?

A

Haemolysis
Hepatocellular damage
Cholestasis

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98
Q

What level of bilirubin classifies clinical jaundice?

A

50mmol/L

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99
Q

What is AST and what should levels be?

A

Aspartate transferase

0-40iu/L

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100
Q

What is ALT and what should levels be?

A

Alanine transferase
5-30 iu/L
Liver specific enzymes

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101
Q

What is ALP and what should levels be?

A

Alkaline Phosphatase

30-120 iu/L

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102
Q

What is GGT and what should levels be?

A

γ-Glutamyltransferase
5-55 iu/L
Levels increase by enzyme inducers

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103
Q

What is albumin and what should levels be?

A

One of the proteins produced by the liver
35-50 g/dL
Lower - oedema

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104
Q

What are PT/INR?

A

Clotting factors produced by the liver

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105
Q

How do we interpret LFT’s?

A

If 2 X ULN then considered abnormal
Trends not isolation
LFTs aren’t always abnormal in patients with cirrhosis
Abnormal LFT’s aren’t always due to liver disease

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106
Q

What are the symptoms of liver disease?

A 
Many asymptomatic
Initially general 
Abdominal pain
Jaundice
Pale stool and dark urine
Pruritus
Spider naevi
Finger clubbing
Bruising and bleeding
Gynaecomastia
Liver palms

In the end stage:
Ascites
Oesophageal and gastric varices
Encephalopathy

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107
Q

What is ascites?

A

Accumulation of fluid in the peritoneal cavity leading to a sowellen abdomen

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108
Q

What is the treatment for ascites?

A 
Fluid/sodium restriction
Diuretics
Daily weight
Daily U+E's
Paracentesis (fluid drained off)
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109
Q

What is Spontaneous Bacterial Peritonitis?

A

Infection of the ascitic fluid without an obvious intra-abdominal source of sepsis

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110
Q

How do you treat Spontaneous Bacterial Peritonitis?

A

Treat with broad spectrum IV antibiotic
3rd gen cephalosporins, co-amoxiclav, tazocin (for at least 5 days)

Norfloxacin/Ciprofloxacin as prophylaxis after iv antibiotic course if getting recurring infections

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111
Q

What is Hepatic Encephalopathy and what are the symptoms?

A

Theories but not clear
Liver not working well so accumulation of toxins, increase BBB permeability, more neurotransmitters int he brain so cause these behavioral changes
Spectrum of neuropsychiatric changes including changes in mood and behaviour, confusion, poor sleep rhythm and eventually delirium and coma

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112
Q

What is the treatment of Hepatic Encephalopathy?

A

Laxatives - for ammonia (Lactulose 20-30ml BD-TDS)
Antibiotics - kill bacteria producing ammonia (Rifaxamin 550mg BD)
Supplement urea cycle

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113
Q

What is portal hypertension and what do varices do?

A

Build up of pressure in portal vein caused by increased resistance to flow and disruption of hepatic architecture and compression of hepatic venules by regenerating nodules
Varicies enable blood to bypass the liver

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114
Q

What happens when varices bleed?

A 
A medical emergency
Vomiting loads of blood
Resuscitation
Endoscopy
Balloon tamponade
Terlipressin iv 1-2mg bolus then every 2-6 hrs until bleeding stops
Octreotide infusion
Antibiotics
PPI
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115
Q

What is secondary prophylaxis for varices bleeding?

A

Propranolol 20-40mg BD
Splanchnic vasoconstriction
Cardiac output results in reduced portal pressures

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116
Q

Why does pruritus occur with liver disease?

A

Build up of bile salts

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117
Q

What is the treatment for Pruritus?

A 
Colestyramine
UDCA
Antihistamines
Topical
Resisant cases - Ondansetron
Rifampicin
Naltrexone, Naloxone
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118
Q

What are the causes of liver disease?

A 
Alcohol
Viral infection
NAFLD
Inherited and metabolic disorders
Immune disease of the liver
Vascular abnormalities
Cancer
Biliary tract disorders
Other infections
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119
Q

What are intrinsic reactions?

A 
Predictable 
Reproducible 
Dose dependent 
Tend to occur rapidly e.g. within hours 
Tend to cause necrosis, acute liver failure
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120
Q

What are idiosyncratic reactions?

A

Not predictable
Not reproducible
Not dose dependent
Tend to take longer to occur
Can result from metabolic idiosyncrasy or immunoallergic reaction
Can cause any type of liver injury e.g. increased LFTs, jaundice, fever, rash, eosinophilia

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121
Q

Examples of idiosyncratic reactions and causative agents

A

Cholestasis – OCP, warfarin, azathioprine, flucloxacillin
ALF – allopurinol, cyclophosphamide, NSAIDS, MDMA, Steatosis – amiodarone, corticosteroids, TPN
Fibrosis and cirrhosis – methotrexate
Vascular disorders – OCP, azathioprine
Acute hepatitis – phenytoin, isoniazid
Chronic hepatitis - isoniazid

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122
Q

What are the symptoms of alcohol withdrawal?

A 
Delirium, marked tremor 
Fear and delusions, restlessness and agitation 
Fever 
Rapid pulse 
Dehydration 
Seizures
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123
Q

What is the treatment for alcohol withdrawal?

A

sedatives and vitamin supplementation
Chlordiazepoxide + Pabrinex IV
Oral vitamin B co strong and thiamine

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124
Q

How does Chlordiazepoxide work in Alcohol withdrawal?

A

Works on GABA receptors to minimise symptoms

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125
Q

Describe Hepatitis A

A 
Most common
Faecal Oral route
Mild, self-limiting
Can clear when young
Doesnt progress to chronic liver disease or carrier status
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126
Q

Describe Hepatitis b

A

Enveloped DNA virus
Highly contagious (blood, saliva, urine, semen, vaginal fluids )
Young more likely to get chronic hep
Leading cause of HCC (hepatic cellular carcinoma)
Diagnose by Hep B surface antigen

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127
Q

What is the treatment of Hep B?

A

Oral antivirals – entecavir or tenofovir LONG TERM
Pegylated Interferon
Aiming for “functional cure” – HBsAg loss, undetectable serum HBV DNA +/- HBsAb seroconversion
Vaccination is available

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128
Q

Describe Hep D

A

Delta virus
Can only replicate in presence of Hepatitis B virus
Acquired in blood, saliva, urine, semen, vaginal fluids
Combination of HBV and HDV increase risk of progression to chronic hepatitis and cirrhosis

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129
Q

What is the treatment for Hep D?

A

Pegylated interferon and oral antivirals as HBV

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130
Q

Describe Hep E

A

Similar to Hep A
Oral-Faecal
Often mild
Doesn’t progress

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131
Q

Describe Hep C

A 
Blood bourne
Six genotypes
Diagnose by antibodies, HCV RNA and genotype 
Many people undiagnosed as asymptomatic
Silent Killer
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132
Q

What is the treatment for Hep C?

A

Curable as doesn’t integrate into cells DNA
Looking for a sustained virological response viral eradicatiom
Finate courses of treatments developed over years
1997-Interferon alpha 2b
2000 – Pegylated Interferon
2001 – Pegylated Interferon and Ribavirin
2011 – First generation directly-acting antivirals (DAAs) – Boceprevir and Telaprevir – added to Pegylated Interferon and Ribavirin regimens
2014 – Second generation DAAs – Sofosbuvir, Sofosbuvir/Ledipasvir, Daclatasvir – “interferonfree” regimens
2015 - Ombitasvir/Paritaprevir/Ritonavir with or without Dasabuvir introduced
2016 – Velpatasvir/Sofosbuvir – “pan-genotypic”, Elbasvir/Grazoprevir introduced
2017 – Sofosbuvir/Velpatasvir/Voxilaprevir and Glecaprevir/Pibrentasvir introduced. Both pan-genotypic

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133
Q

What is the difference between Crohns and UC?

A

Crohns- Whole of GI tract from mouth to anus can be affected-patchy
UC - mucosa of colon and rectum - diffuse

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134
Q

What are the causes of IBD?

A 
It is not fully understood
Genetic
Envrionmental
Immunological factors
Gut microbes
Smoking
Infection 
Diet
Medication
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135
Q

IBD symptoms

A 
Abdominal Pain
Diarrhoea - watery, bloody, mucus
Tiredness and fatigue
Urgency
Weight loss
Anaemia
Fever
Nausea and vomiting
Abdominal bloating and distension
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136
Q

IBD extra-intestinal manifestation

A

Swollen joints-arthritis
Eye problems - episcleritis, iritis, uveitis
Erythema nodosum – swollen fat under skin causing redness, bumps and lumps
Pyoderma gangrenosum – skin ulceration
Primary sclerosing cholangitis

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137
Q

What are strictures and fistulas and what do they occur in?

A

Strictures - narrowed segments of bowel causing blockages, acute dilation and perforation
Fistulas - new little abnormal channels forming lined with granulation tissue

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138
Q

What investigations are doe for IBD?

A 
Blood tests
Stool cultures (rule out C diff ect)
Coeliac screen
Faecal calprotectin
Abdominal imagine
Endoscopy including capsule endoscopy
Colonoscopy
Bisopises take to differentiate
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139
Q

Which index is used to classify UC?

A

Truelove and Witt’s

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140
Q

Which index is used to classify Crohns?

A 
Looks at lots of different parameters:
Number of liquid or soft stools 
Severity of abdominal pain 
General well-being 
Presence of complications  
Fever 
Use of loperamide 
Presence anaemia 
Body weight 
Abdominal mass absent or present
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141
Q

Are drugs used to get IBD patients into remission used whilst they are in remission?

A

No - they aren’t good at maintaining remission

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142
Q

Why do IBD drugs require a lot of monitoring?

A

They target the immune system

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143
Q

Are drug treatments for Crohns and UC the same?

A

There is some overlap but no as different parts of the GIT are affected

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144
Q

Is one drug used to treat IBD?

A

No, often a combination of drugs is used

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145
Q

Which formulation goes furthest into the colon?

A

Enema>foam>suppository

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146
Q

What are the treatments for IBD?

A 
Antibiotics if infection/complication
Corticosteroids
Aminosalicylates
Immunomodulating agents
Antibiotics
Novel treatments
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147
Q

Which corticosteroids are used for IBD? What doses are given?

A

Prednisolone
Hydrocortisone
Budesonide

Prednisolone 40mg OD, reduced by 5mg/week

If acute-severe, iv hydrocortisone 100mg QDS in hospital then switch to oral prednisolone

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148
Q

Which aminosalicylates are used for IBD?

A

Sulfasalazine
Mesalazine
Balsalazide
Olsalazine

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149
Q

Which immunomodulating agents are used for IBD?

A

Thiopurines – Azathioprine and Mercaptopurine
Methotrexate, Ciclosporin, Tacrolimus
Biologics – Infliximab, Adalimumab, Vedolizumab, Ustekinumab

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150
Q

Which novel treatments can be used for IBD?

A

Faecal Microbiota Transplant

Probiotics

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151
Q

How are corticosteroids used in IBD?

A

Induce remission but do not prevent progression of disease or development of complications
Dampen inflammatory reaction so you can add another drug to aid remission

If flare up is severe, give iv

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152
Q

What are the disadvantages of corticosteroids?

A

Side effects
Infection risk
Osteoporosis risk
Steroid treatment card

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153
Q

Can you give oral and topical preps of aminosalicylates together?

A

Yes

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154
Q

What types of topical (rectal) aminosalicylate preparations are available?

A 
Suppositories 
Foams 
Enemas 
Tablets 
Granules
155
Q

What was the first aminosalicylate to be used for IBD and what were the problems?

A

Sulfasalazine
Side effects - headache, nausea, rashes
These limited the dose you could use

156
Q

What are the newer aminosalicylates called?

A

Balsalazide
Olsalazine
Mesalazine

157
Q

Why can’t you switch brands of mesalazine?

A

They all release in different places in the GIT

158
Q

What are the side effects of aminosalicylates?

A

Arthralgia, abdominal pain, diarrhoea, dizziness

Blood dyscrasias

159
Q

What is important to monitor when giving aminosalicylates?

A 
Renal function (baseline, 3 months then annually – more frequent if impairment) 
Blood dyscrasias
160
Q

Why might thiopurines be used?

A

If you can’t get control on steroids - first line immunomodulators for IBD
Induce and maintain remission
Steroid sparing
3-6 months for full effects

161
Q

Azathioprine is a pro-drug, what is it converted to? What happens to this?

A

Mercaptopurine
Then converted to TGN (active metabolite)
TMPT then converts to MeMP (not active and can cause side effects)

162
Q

What is the dose of thiopurines?

A

Azathioprine - 2-2.5mg/kg/day

Mercaptopurine - 1-1.5mg/kg/day

163
Q

What measurements must be done for thiopurine treatment and what do they mean?

A

TMPT levels - prior to, repeated one month after or if not responding to treatment
Low - reduce dose (risk myelosuppression)
High - risk hepatotoxicity as more going down this metabolic pathway

Full blood count weekly (4 weeks) then at least every 3 months

164
Q

What are the side effects of thiopurines?

A

Hypersensitivity reaction – immediate withdrawal
Myelosuppression (bone marrow suppression)
Neutropenia and thrombocytopenia
GI – nausea, vomiting, diarrhoea
Liver disorders

165
Q

When is Methotrexate used in IBD and what must it be prescribed with?

A

For maintainance if Azathioprine can’t be used

Co-prescription of folic acid

166
Q

Why is Tacrolimus used is IBD?

A

Can induce remission in mild-mod UC if not responsive to other treatments

167
Q

Why is Ciclosporin used is IBD?

A

To induce remission in severe-acute UC refractory to steroids

168
Q

What are biologics, how do they work and give examples

A

Monoclonal antibodies
Bind to cytokine - Tumour Necrosis Factor-α (TNF- α) and inhibit inflammatory effects
Infliximab and Adalimumab
Ustekinumab and Vedolizumab

169
Q

Why are steroids given pre treatment for Inflicimab?

A

Murine and human amino acid sequences so can get an infusion related reaction

170
Q

What future therapies are being considered for IBD?

A

Faecal Microbiota Transplant
Probiotics
New biolohics
Small molecule inhibitors of RNA and intracellular cytokine pathways

171
Q

Give examples of elective (non emergency) surgical procedures for IBD

A 
Bowel resection 
Strictureplasty 
Colectomy 
Proctocolectomy with ileostomy 
Fistula treatment 
Abscess drainage
172
Q

What should be co prescribed with corticosteroids and why?

A

Calcium and vitamin D to prevent osteoporosis

173
Q

What are the routes of administration fo Infliximab and Adalimumab for IBD?

A

Infliximab - iv infusion

Adalimumab - sc injection

174
Q

What are the risks of Infliximab and Adalimumab for IBD?

A

Lymphoma/malignancy

175
Q

What does Ustekinumab for IBD target and how is it given? What are the risks?

A

Blocks IL-12 and IL-23-Inhibits inflammatory effects in gut
Initial IV infusion then SC injection
Risk of reactivation of infections and malignancy

176
Q

What does Vedolizumab for IBD target and how is it given? What are the risks?

A

Leucocyte adhesion inhibitor
IV infusion
Risk of reactivation of infections and malignancy

177
Q

How is a Faecal Microbiota Transplant thought to work?

A

Composition of gut microbes thought to be abnormal so we try and replace this
Use a healthy donor and transfer gut microorganisms into intestinal tract of recipient via colonoscopy or ec tablets
Clinical trials ongoing

178
Q

Which IBD complications require immediate surgery?

A 
Intestinal blockage
Bleeding 
Perforation
Fistula
Abscess
Toxic megacolon
179
Q

What is the definition of diarrhoea?

A

Not strict definition
A change in bowel habits for that person
More frequent and looser stools

180
Q

How can diarrhoea be categorised?

A

Acute - < 14 days
Persistent - > 14 days but less than 28 days
Chronic > 28 days

181
Q

What is the pathophysiology of diarrhoea?

A 
Increased osmotic load in gut lumen 
Increase in secretion 
Inflammation of intestinal lining 
Increased intestinal motility
(can be more than one)
182
Q

What can cause acute diarrhoea? Give examples

A 
Infection or ingestion of toxins
Bacterial e.g. Campylobacter, Escherischia coli, Salmonella 
Viruses e.g. rotavirus or norovirus 
Drug
Parasites
Anxiety
183
Q

How long does acute diarrhoea last?

A

Most cases are self limiting and resolve within 72 hours

184
Q

What is travellers diarrhoea and how long does it last?

A

Experienced by travellers or holiday
Usually within the first few days of trip
Can last a bit longer but usually resolves within 7 days
Some infections (e.g. giardiasis and amoebic dysentery) can cause persistent or recurrent diarrhoea or systemic complications

185
Q

What are the causes of travellers diarrhoea?

A

Enterotoxigenic Escherichia coli (ETEC), Campylobacter
Salmonella
Enterohaemorrhagic E coli and Shigella,
Viruses, protozoa and helminths

186
Q

What are the symptoms of travellers diarrhoea?

A

Same as acute diarrhoea but can also have bloody diarrhoea (dysentery)

187
Q

What is the treatment for travellers diarrhoea?

A

More symptomatic relief as per acute.
So antibiotic prophylaxis rarely recommended
Hygiene, food and drink advice give:
wash hands - soap
Antiseptic wipes/gel
Avoid local water even for teeth
Avoid ice cubes, dairy products, ice cream, home distilled drinks and salads
Fresh foods- cook, boil, peel
Avoid fish and shellfish unless fresh and sure uts not been near sewage
Clean, hygenically run esablishments

188
Q

What is chronic diarrhoea?

A

Recurrent or persistent diarrhoea

189
Q

What are the causes of chronic diarrhoea?

A

IBS
IBD
Malabsorption syndromes (e.g. coeliac disease, lactose intolerance)
Metabolic disease (e.g. diabetes, hyperthyroidism)
Laxative abuse

190
Q

What questions about symptoms of diarrhoea must you ask?

A 
Stool frequency 
Nature e.g. blood, mucus 
Occurrence – isolated or recurrent 
Duration 
Onset 
Timing 
Food 
Recent travel 
Medication
191
Q

When should you refer adults?

A 
> 72 hours in healthy adults 
> 48 hours in elderly
> 24 hours if diabetic
Associated severe vomiting and fever 
History of change in bowel habit 
Blood or mucus in stools
Suspected ADR
Alternating diarrhoea and constipation in elderly 
Weight loss 
Recent hospital treatment or antibiotic treatment 
Evidence of dehydration
Severe pain/rectal pain
192
Q

What is given to prevent dehydration?

A 
Oral Rehydration Therapy 
Loperamide 
Morphine 
Diphenoxylate 
Adsorbents 
Antibiotics
193
Q

What should Oral Rehydration Solutions do?

A

Enhance the absorption of water and electrolytes
Replace electrolyte deficit adequately and safely
Contain alkalinising agent to counter acidosis
Prevent the possible induction of osmotic diarrhoea - slightly hypo-osmolar (about 250 mmol/litre)
Simple to use in hospital and at home
Palatable and acceptable, especially to children
Readily available

194
Q

What does Oral Rehydration Therapy contain and why?

A

Sodium and potassium-to replace essential ions
Citrate and/or bicarbonate-to correct acidosis
Glucose or another carbohydrate e.g. rice starch

195
Q

What is the usual ORT dose?

A

200-400ml after very loose motion

196
Q

How does loperamide work for diarrhoea?

A

Synthetic opioid analogue - µ (mu) opioid receptor agonist
Direct action on opiate receptors in the gut wall
Inhibits gut peristalsis

197
Q

What is the adult dose of loperamide?

A

Initially 4 mg (2 caps), followed by 2 mg for up to 5 days, dose to be taken after each loose stool; usual dose 6–8 mg daily; maximum 16 mg per day.

198
Q

What are the contra-indications for loperamide?

When should it be avoided?

A

Active ulcerative colitis
Antibiotic associated colitis
Conditions where inhibition of peristalsis should be avoided
Conditions where abdominal distension develops

Avoid:
Bloody/suspected inflammatory diarrhoea
Significant abdominal pain

199
Q

What are the side effects of loperamide?

A

Abdominal cramps
Dizziness
Serious cardiac adverse reactions associated with high doses

200
Q

When should antibiotics be given for diarrhoea?

A

Only when there is a confirmed infection - stool sample taken and causative organism identified first
Can use in severe infection (fever > 39oC and prolonged symptoms, in the elderly or immunocompromised)

201
Q

What can be caused by reliance on loperamide?

A

Risk antimicrobial resistance
Prolong symptoms as many cause GI side-effects
Pre-dispose to Clostridium difficile
Worse diarrhoea

202
Q

Why is morphine sometimes given for diarrhoea? What weight content is it?

A

Direct action intestinal smooth muscle

0.5-1mg - debated if it is effective for diarrhoea

203
Q

Why is Diphenoxylate sometimes given for diarrhoea? What form does it come in? Why are people put off from taking high doses to get opioid effect?

A

Synthetic derivative of pethidine – opioid effect to slow gut
Comes as a combination product:co-phenotrope (diphenoxylate hydrochloride 2.5mg/atropine 25mcg)
Side effects in high amounts

204
Q

Why are Adsorbants sometimes given for diarrhoea? Given examples

A

Adsorb microbial toxins and micro-organisms in gut and flushes out

Kaolin (Kaolin and Morphine)
Bismuth subsalicylate

205
Q

What lifestyle advice should a pharmacist give for a patient with diarrhoea?

A 
Plenty of clear fluids 
Avoid drinks high in sugar 
Avoid milk and milky drinks 
Eat light, easily digested food 
Gastroenteritis – infections. Precautions including not returning to work until symptom free for 48 hours, hygiene advice and cleaning of sanitary equipment 
Check meds as absorption can be reduced
206
Q

What is the rotavirus vaccine?

A

A live, oral vaccine that protects young children against gastro-enteritis caused by rotavirus infection.

207
Q

Is the rotavirus vaccine on the childhood immunisation schedule?

A

Yes

208
Q

What is the rotavirus vaccine schedule?

A

the first at 2 months of age, (must be given between 6–14 weeks of age)
the second at 3 months of age
the second dose should be given after an interval of at least 4 weeks
Course should be completed before 25 weeks of age

209
Q

How many people have C diff naturally?

A

2-3% of the adult population

210
Q

What can C diff lead to?

A

Pseudomembranous colitis

211
Q

How does C diff become harmful?

A

Had antibiotics that have killed of normal gut flora so environment there is supportive of C diff growing – also need spore there
(May already have or may acquire spore from the hospital)
C diff needs to produce particular toxin and not all C diff’s produce this toxin

212
Q

What are risk factors for CDI infection?

A 
Antimicrobial choice
Antimicrobial duration
Acid-suppressing medicines
Age - co-morbidities
Length of stay
Recent hospitalisation
213
Q

How is C diff managed?

A

Depends onseverity
STOP antimicrobials and acid supressing med if possible
Stop antimotility meds
Maintain adequate fluid balance
Targeted C diff treatment
Infection control - alcohol gels and isolation

214
Q

Which antimicrobial treatments are given for C diff?

A 
Oral metronidazole - first line (mild-mod)
Oral vancomycin (severe or mild-mod)
Oral fidaxomicin (severe recurrent or risk of recurrent)
215
Q

What is the dose of oral metronidazole for CDI?

A

400mg TDS for 10-14 days

216
Q

What is the dose of oral Vancomycin for CDI?

A

125mg every 6 hours

can give up to 500mg every 6 hours

217
Q

What is the dose of oral fidaxomicin for CDI?

A

200mg BD for 0 days

218
Q

What is given to treat CDI if critically unwell?

A

Combination therapy of IV Metronidazole and oral Vancomycin

Iv

219
Q

What non-antimicrobial treatments for CDI are there?

A

Probiotics
Faecal Microbiota Transplant
Intravenous Immunoglobulin

220
Q

What is constipation?

A

Passage of hard stools less frequently than normal
Typically less than three bowel movements in one week
But varies between people

221
Q

Who does constipation affect?

A

All people of all ages

More common in women, especially if pregnant, and older people

222
Q

What are the symptoms of constipation?

A 
Abdominal discomfort and distension 
Abdominal cramping 
Bloating 
Nausea
Difficulty passing stool
223
Q

What is functional (idiopathic) constipation?

A

No anatomical or physiological cause known

224
Q

What is secondary constipation?

A

Induced by a particular condition or medicine

225
Q

Which non-medical factors pre-dispose to constipation?

A 
Inadequate fluid intake 
Inadequate dietary fibre 
Dieting 
Changes in lifestyle 
Suppressing the urge to defecate
226
Q

Which medical factors pre-dispose to constipation?

A 
Coeliac disease 
Depression 
Diabetes 
GI obstruction 
IBS
Parkinson’s disease 
Hypercalcaemia 
Hypokalaemia 
Hypothyroidism
227
Q

Which medications can cause constipation? Give examples

A

Antacids containing aluminium and calcium
Antihypertensives – diuretics, calcium channel blockers
Antidepressants – tricyclics and some monoamine oxidase inhibitors
Antimuscarinics – procyclidine, oxybutynin
Antiparkinsonian medicines – levodopa, dopamine agonists, amantadine
Opioid analgesics
Iron

228
Q

What should an opioid be co prescribed with?

A

A laxative

229
Q

What should a patient with constipation be assessed for?

A

Bowel habit
Examination
Try to identify cause
Rome III diagnostic criteria

230
Q

What are the aims of treatment for constipation?

A

Restore normal frequency defecation
Achieve regular, comfortable defecation
Avoid laxative dependence
Relieve discomfort

231
Q

What are the treatments for constipation?

A

Change primary cause - diet, fluids, lifestyle

Laxatives

232
Q

What are the 4 types of laxatives?

A

Bulk-forming
Stimulant
Osmotic
Faecal-softening

233
Q

How do bulk-forming laxatives work?

A

Increase faecal mass through water binding to stimulate peristalsis

234
Q

How long do bulk-forming laxatives take to work?

A

Take several days for full effect

235
Q

What must the patient do for bulk-forming laxatives to work?

A

Maintain a good fluid intake as they work through water binding

236
Q

Can bulk-forming laxatives be used long term?

A

In people prone to constipation (elderly)

237
Q

Give examples of bulk-forming laxatives

A

Ispaghula husk

Methylcellulose (also a softener)

238
Q

How do stimulant laxatives work?

A

Increase intestinal motility via muscle contractions

Work on cells in smooth muscle to stimulate peristalsis

239
Q

How long do stimulant laxatives take to work?

A

A few hours - take before bedtime, will work by morning

240
Q

What can stimulant laxatives cause?

A

Abdominal cramps

Prolonged use - diarrhoea, fluid and electolyte imbalance

241
Q

Give examples of stimulant laxatives

A

Senna
Bisacodyl
Dantron (terminal illness)

242
Q

How do osmotic laxatives work?

A

Work within colonic lumen to retain and draw water into intestine by osmosis and stimulate peristalsis

243
Q

What must the patient maintain for osmotic laxatives to work?

A

A good fluid intake

244
Q

What types of osmotic laxatives are there and how long do they take to work?

A

Macrogel powders: 1-3 days
Lactulose: 2-3 days
Phosphate enema or suppository: 15-30 mins
Magnesium hydroxide sachets: 3-6 hours

245
Q

What are magnesium hydroxide sachets used as a laxative for?

A

Clearing prior to bowel procedures

e.g. colonoscopy

246
Q

How do faecal softening laxatives work?

A

Stimulate peristalsis by increasing faecal mass: they lower surface tension and allow water and fats to penetrate faeces

247
Q

Give examples of faecal softening laxatives and how long do they take to work?

A

Docusate sodium: 1-3 days

Gylcerol suppository: within 1 hour

Arachis oil enema: within 30 mins

248
Q

When must an Arachis oil enema not be used?

A

If the patient has a nut allergy

249
Q

What complications can constipation cause?

A

Faecal impaction
haemorrhoids
Rectal prolapse
Anal fissures

250
Q

What is Coeliac disease?

A

Autoimmune condition affecting the small bowel
Genetic predisposition
Body’s immune system attacks itself when gluten is eaten – thinks gluten is foreign material
Reaction varies between people
BUT NOT ALLERGIC REACTION - NO ANAPHYLACTIC SHOCK

251
Q

How is Coeliac disease diagnosed in adults?

A

Serology - look at levels of immunoglobulins person to person
Endoscopy for SI biopsy
(Repeat biopsy on gluten-free diet)
(Gluten challenge (>10g per day, 6/52)

252
Q

What are the symptoms of coeliac disease?

A

Not every person has symptoms and they vary person to person - mild to severe

Headaches
Diarrhoea
Abdominal pain
Lethargy

253
Q

How long do symptoms of Coeliac disease last?

A

Few hours to a few days

254
Q

Coeliac disease is a ‘multi-system disorder’ - what does this mean?

A

symptoms can affect any area of the body and lead to other conditions

255
Q

What complications can Coeliac disease cause?

A

Long term malabsorption and osteoporosis
Refractory coeliac disease – symptoms WITH gluten free diet
Ulcerative jejunitis
Enteropathy associated T cell lymphoma
Autoimmune disease

256
Q

What happens the longer you continue to eat gluten with Coeliac disease?

A

The more you risk triggering another autoimmune disease

257
Q

Is there a cure for Coeliac disease? What happens if you reintroduce gluten? What is being developed?

A 
No cure 
Lifelong gluten free diet
Reintroduce gluten=immune system reacts and gut lining becomes damaged again
Research underway to develop a vaccine
Looking at modifying the immune system
258
Q

What is included in a gluten free diet?

A

Fresh meat, fish, cheese, eggs, milk, fruit and vegetables (watch for contamination)
Specially-manufactured wheat starch

259
Q

Why do patients not like gluten free diets?

A 
Taste
Expensive 
Difficult to eat out 
No agreed international consensus on permissible levels 
Range of symptoms with ingestion 
Nutritional aspects
260
Q

What can be given on prescription for Coeliac disease?

A

Bread and flour mixes only

261
Q

What is IBS?

A

Chronic condition
At least 6 months of abdominal pain and bowel symptoms (diarrhoea, constipation or combination of both)
Cause unclear and can differ patient to patient

262
Q

What is the treatment for IBS?

A

Poorly understood so cant treat underlaying cause
Treatment aimed at symptomatic relief:
Dietary changes and exercise
Antispasmodics (e.g. mebeverine, hyoscine, peppermint oil)
Anti-diarrhoeal (e.g. Loperamide short courses)
Laxatives (e.g. bulk-forming, stimulant, osmotic)
Probiotics

263
Q

Is one treatment given for IBS?

A

No, may have different symptoms at different times so swap treatments around

264
Q

Why are antispasmodics given for IBS?

A

They relax smooth muscle
They are well tolerated
Peppermint oil capsules can also be used TDS

265
Q

Which antispasmodic is the most common for IBS in the UK and what formulation and dose?

A

Mebeverine MR capsule

200mg BD

266
Q

Why is there an extensive blood flow to the kidneys?

A

Served by renal artery and renal vein

267
Q

What are the two distinct areas when you cut through the kidneys?

A

Outer - cortex (brown)

Inner - medulla (dark grey)

268
Q

Where are the kidneys attached to?

A

The back of the abdominal wall (NOT in peritoneal cavity)

269
Q

How do kidneys maintain homeostasis?

A

Regulate blood volume/pressure
Osmolarity - maintain iron levels
Acid base balance

270
Q

What do the kidneys excrete?

A

Metabolites (urea which is a product of AA breakdown)

Ingested chemicals, drugs

271
Q

What is the endocrine function of the kidney?

A 
Erythromycin hormone involved in RBC production
Vitamin D3 (Ca2+ homeostasis)
272
Q

What can happen if Low vitamin D3 levels occur?

A

Rickets - softer bones which bend under pressure

273
Q

What are the two arterioles in the nephron and which is bigger? why?

A

Afferent arteriole - bigger
Efferent arteriole

Afferent bigger to increase pressure to aid filtration into bowmans capsule

274
Q

What is the route of the blood in the nephron?

A

Blood - afferet arteriole - glomerulus - (some filtrates into bowmans capsules) - efferent arteriole

275
Q

What is the vasa recta?

A

The capillaries surrounding the nephron

276
Q

Describe filtration in the kidney

A

Molecules from plasma into Bowman’s Capsule

277
Q

Describe secretion in the kidney

A

Molecules secreted from vasa recta peritubular capillary INTO the tubule (then pass out into urine)

278
Q

Describe reabsorption in the kidney

A

Valuable compounds back into blood from the nephron

279
Q

What are the three layers of the capillary and how are they arranged?

A

Capillary endothelium stcik to a basement membrane made of proteins and carbs, with capsule cells (podocytes) wrapped around the capillary

280
Q

What happens to large molecules vs small molecules in the capillary?

A

Large -pass straight through capillary
Small - filtered and pass straight through gaps (blood vessels are leaky, and gaps occur between cells and between podocytes)

281
Q

Approx. what size molecules pass through pores in Bowman’s capsule?

A

30 kPa and smaller

282
Q

What does a larger molecule in the urine indicate?

A

The kidney is damaged

283
Q

Some drugs can bind to proteins, what effect does this have on filtration?

A

They are not filtered, unlike some drugs that are unbound and pass to urine

284
Q

Give an example of a drug that is extensively bound to proteins?

A

Warfarin = 99% bound

285
Q

What is the glomerular filtration rate?

A

Volume of fluid filtered per unit time (per hour or day)

Measure of how well the kidneys are functioning

286
Q

What can affect GFR?

A

Drastic changes

e.g. kidney stones, polycystic kidney disease

287
Q

What happens to GFR as CKD worsens?

A

GFR decreases

288
Q

Give examples of molecules filtered in the kidney

A

Water, ions, drugs

289
Q

Which diseases can affect renal function?

A

Kidney cancer
Kidney cysts
Obstructive kidney stones

290
Q

What do changes in renal function alter?

A

Elimination

291
Q

Which factors affect renal function?

A

Age

Disease

292
Q

If there is reduced renal function, what must happen to drug doses and why?

A

Reduce the dose
Not as much drug being cleared
Higher levels in the body
Can result in toxicity

293
Q

How do you measure renal function?

A

Measure Glomerular Filtration Rate

294
Q

What is GFR?

A

Rate at which fluid in the plasma is filtered

295
Q

How can Inulin be used to measure renal function?

A

Administered IV
Polymer of fructose and freely filtered
Not reabsorbed nor secreted by the nephron/metabolised by kidney so amount of inulin filtered is the amount excreted in the urine

296
Q

How can Creatine be used to measure renal function?

A

Produced by muscles and freely filtered

How much in urine = how much has been filtered + 10% that has been secreted by the nephron

297
Q

What is renal clearance?

A

Volume of plasma from which a substance is completely removed per unit time

298
Q

Which three measurements are needed to calculate renal clearance?

A 
V = rate urine production (vol/time)
[Ux] = urine conc of x
[Px] = plasma conc of x
299
Q

Which transporters are involved in renal drug elimination?

A 
OAT
OATP
OCT
MRP
BCRP
P-gp
300
Q

Is glucose found in the urine of healthy individuals?

A

No - negligible

301
Q

Which uptake and efflux transporters does Methotrexate use?

A

Uptake - OCT1, OAT1

Efflux - MRP2, MRP4, ABCG2

302
Q

Which uptake and efflux transporter do Pitvastatin and rosuvastatin use?

A

Uptake - OAT3

Efflux - ABCG2

303
Q

Which uptake and efflux transporter does Fexofenidine use?

A

Uptake - OAT3

Efflux - ABCB1

304
Q

Which uptake and efflux transporter does Digoxin use?

A

Uptake - OATP1

Efflux - ABCB1

305
Q

Why might you inhibit glucose transporters?

A

To treat diabetes

Plasma levels of glucose in the blood will drop

306
Q

Which transporter should be inhibited to inhibit glucose transport?

A

SGLT2 found in kidney

307
Q

Give example of a SGLT2 inhibitor

A

Dapagliflozin (Forxiga)

308
Q

How much filtered Na+ is reabsorbed in the proximal tubule?

A

70%

309
Q

When Na+ is reabsorbed, what follows?

A

Water by passive diffusion

310
Q

What is Na+ uptake coupled to?

A

H+ secretion

311
Q

What is also produced during the acid base balance and what does this do?

A

HCO3- (carbonic acid)

Acts as a buffer

312
Q

How are the kidneys and lungs linked?

A

Via the circulatory system

313
Q

What can inefficient (diseased) lungs lead to?

A

Respiratory Acidosis (Build up of protons in the plasma)

314
Q

How do kidneys prevent respiratory acidosis?

A

Increase proton secretion

315
Q

How can changes in pH alter renal drug handling?

A

pH affects ionisation of drug and therefore membrane permeability

316
Q

Which steroid hormone increases Na+ reabsorption in the kidney?

A

Aldosterone

317
Q

Where is aldosterone produced?

A

Outer cortex of the adrenal gland

318
Q

What does aldosterone do?

A

Increased Na+ channels in the apical membrane

Increases Na, K pumps in the basolateral membrane

319
Q

Which system controls aldosterone secretion?

A

The renin-angiotensin system

320
Q

How does the renin angiotensin system work?

A

Low Na in the body – sensed by cells in the kidney
Cells produce renin in response
Renin converts Angiotensinogen to Angiotensin I which is inactive
Angiotensin I comes into contact with Kidney and lung
Capillary cells
ACE converts AGI to AGII
AGII circulates until it gets to adrenal cortex and tells it to make aldosterone

321
Q

What are ACE inhibitors used for and give two examples

A 
Heart failure (+ diuretic)
High blood pressure

e.g. Captopril. fosinopril

322
Q

What is the indication for diuretics, what are they used for and give two examples

A

Oedema, hypertension, congestive heart disease
To increase the amount of water lost through the kidneys

e.g. Spironolactone, Amiloride

323
Q

How does Spironolactone work?

A

It is an aldosterone analogue
Binds to same receptor so aldosterone cannot bind and trigger response
Less channels and pumps - more sodium and water passes out of the body

324
Q

How does Amiloride work?

A

Na+ channel blocker

Binds to sodium channels in apical membrane so more sodium and water stays in the fluid and is passed out of the body

325
Q

How much blood does the kidney filter daily?

A

120L

326
Q

How much filtrate from the kidney is reabsorbed?

A

99%

327
Q

How much filtrate from the kidney is lost in the urine daily?

A

1.5L

328
Q

For what reasons my there be a reduced number of nephrons (<1.4 million)?

A

Hypertensive patients

Reduced with age

329
Q

How much Na+ reabsorption occurs in the proximal tubule and via which exchanger?

A

60-70%

Na+/ H+ exchanger

330
Q

Explain the counter current multiplier in the LoH

A

Concentration of interstitial fluid increases as LoH descends so osmotic potential increases

331
Q

How much Na+ is actively reabsorbed in the thick ascending LoH and via which transporter?

A

20-30%

Na/K/Cl transporter

332
Q

Do cells in the thick ascending LoH have a high or low permeability to water?

A

Low permeability

333
Q

Do cells in the distal convoluted tubule have a high or low permeability to water?

A

Impermeable to water

334
Q

How much Na+ is reabsorbed in the distal convoluted tubule?

A

7%

335
Q

What happens in the collecting tubule?

A

ADH binding to the vasopressin receptors in aquaporin channels causes their insertion into the apical membrane. Can remove as much as 15% of filtered water, making the urine considerably hypertonic to plasma.
Na+ reabsorption mediated by aldosterone occurs

336
Q

How do diuretics increase excretion of Na+ and water?

A

through direct action on nephron cells or changing composition of the filtrate

337
Q

How do loop diuretics work?

A

Inhibit Na+/K+/2Cl- carrier in thick ascending limb

They cause vasodilation before the onset of diuresis

338
Q

Give examples of loop diuretics

A

Furosemide
Bumetanide
Torasemide

339
Q

How are loop diuretics thought to cause vasodilation?

A

Angiotensin II usually constricts arteries but loop diuretics reduce response to diuretics
Increased vasodilating PG’s present
endogenous Na+/K+/ATP inhibitor decrease

340
Q

What effect to NSAIDs have on loop diuretics?

A

NSAIDs ↓ diuretic action of furosemide (PG inhibition/ competition for OAT)

341
Q

What are the indications for loop diuretics?

A 
Acute pulmonary oedema
Chronic heart failure
Liver cirrhosis + ascites
Nephrotic sysndrome
Renal failure
Hypertension (+reduced renal function)
Hypercalcaemia
342
Q

Side effects of loop diuretics

A 
Hypotension
Hypokalaemia
Metabolic alkalosis
Gout
Hearing loss
343
Q

Why is there a loss of potassium with loop diuretics?

A

Increase in sodium which enters collecting duct – drives sodium potassium exchange pump
Increase in potassium entering epithelial cells the and increase in potassium leakage into filtrate/urine
large conc of Na+ remaining in filtrate (because ther is less reabsorption in LoH) → drives Na+/K+ pump

344
Q

Where are loop diuretics absorbed?

A

Through the GI tract

Furosemide absorbed in stomach/ upper small intestine

345
Q

How are loop diuretics administered?

A

Orally/iv

346
Q

How long until the peak effect of loop diuretics occurs?

A

<1 hr orally

30 minutes iv

347
Q

What do loop diuretics bind to and what problems can this have if the glomerulus is damaged?

A

Albumin

If glomerulus is damagesd, less protein available to bind to so have to give more which causes more side effects

348
Q

How do loop diuretics reach their site of action?

A

Via PCT excretion

349
Q

How are loop diuretics excreted?

A

In urine - they enter the filtrate

350
Q

What is the half life of loop diuretics?

A

90 minutes

351
Q

What do thiazide like diuretics act on?

A

Inhibit Na+/ Cl- cotransporter – blocking sodium reabsorption

352
Q

Why are thiazide like diuretics less effective than loop?

A

They act on the distal tubule but more Na reabsorption occurs in the ascending LoH

353
Q

Give examples of thiazide like diuretics

A

Chlortalidone
Inapamide
Metolazone
Bendroflumethiazide

354
Q

What can a low dose of thiazide diuretics produce?

A

A vasodilator effect

355
Q

Why is the effect of thiazide diuretics over time limited?

A

Renin angiotensin system kicks in - increases blood pressure

356
Q

What are the indications for thiazides?

A

Hypertension
Mild to moderate heart failure
Oedema treatment
Nephrogenic diabetes insipidus

357
Q

Are loop or thiazide diuretics better tolerated?

A

Thiazide-like diuretics better tolerated than loop diuretics

358
Q

Side effects of thiazide like diuretics

A

Increase urinary frequency
Erectile dysfunction
Hypokalaemia
Impaired glucose tolerance

359
Q

How can you reduce K+ depletion?

A

Increase intake in diet - fruit juice, instant coffee, bananas
Give K+ supplements alone or combined with the diuretic
Use K+ sparing diuretics

360
Q

Can thiazide-like diuretics be given orally and iv?

A

No just orally

361
Q

How are thiazide-like diuretics excreted?

A

In urine

362
Q

What is the dose, peak effect and duration of Bendroflumethiazide?

A

2.5mg daily
Peak 4-6 hrs
Duration
8-12 hrs

363
Q

What is the dose of Chlortalidone and what is this medicine?

A

25mg daily

A thaizide-like diuretic

364
Q

How do Potassium-sparing diuretics work?

A

They are aldosterone agonists so block Na+ reabsorption and Na+/K+ exchange in collecting tubule

365
Q

Give examples of Potassium-sparing diuretics

A

Spironolactone

Eplerenone

366
Q

What are the indications for Spironolactone?

A

Primary hyperaldosteronism
Ascites caused by liver cirrhosis
Oedema
Severe heart failure

367
Q

What are the indications for Eplerenone?

A

Adjunct in patients with left ventricular failure after MI

368
Q

What are the side effects of K+ sparing diuretics?

A

Hyperkalaemia
GI upset
Gynaecomastia (more with spironolactone)
Menstrual disorders/testicular atrophy

369
Q

Where is spironolactone absorbed from?

A

The gut

370
Q

What is spironolactone metabolised to and how long is the half life?

A

Canrenone

Half life = 16 hrs

371
Q

Does spironolactone have a fast or slow onset of action?

A

Slow

372
Q

Does Eplerone have a shorter pr longer elimination half life than spironolactone?

A

Shorter

373
Q

Does Eplerone work for longer or less time than spironolactone?

A

Less time

374
Q

Why do Triamterene + amiloride have limited efficacy as diuretics?

A

Block Na+ channels in the collecting tubules, where there is little sodium reabsorption

375
Q

What are the side effects of Triamterene + amiloride?

A

Hyperkalaemia

Not safe to use in patients with renal impairment or on drugs which increase potassium

376
Q

What happens to Triamterene and how is it best administered?

A

Partially metabolised in liver

Well absorbed orally

377
Q

How is Amiloride excreted in the urine?

A

Unchanged

378
Q

Which two drugs are in Co-amilofruse and what is it used for?

A

Amiloride and Furosemide

Oedema

379
Q

Which two drugs are in Co-amilozide and what is it used for?

A

Amiloride and hydrochlorothiazide

Hypertension/ congestive HF/ oedema

380
Q

How do osmotic diuretics work?

A

They increase the osmolarity of filtrate - draw water in

Increase excretion of water and Na+

381
Q

Give and example of an osmotic diuretic

A

Mannitol

382
Q

Where do osmotic diuretics act?

A

PCT, ascending LoH and CD

383
Q

What are the indications for osmotic diuretics?

A

Cerebral oedema
Raised intra-ocular pressure
Acute renal failure
Given with loop/ thiazide diuretics to maintain K+ balance

384
Q

What are the side effects of osmotic diuretics?

A

Hyponatraemia
Headache
Nausea + vomiting

Sem 2 year 2 (9 decks)

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