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Pharmacology Flashcards

1
Q

What is nausea

A

Highly, unpleasant sensation felt in the throat as a sinking sensation. Often relieved by vomiting

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2
Q

What does nausea usually precede

A

Vomiting

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3
Q

What is retching

A

Retroperistalsis of the stomach and oesophagus without vomiting

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4
Q

Does stomach contraction cause vomiting (emesis)

A

No as stomach, oesophagus and associated sphincters relax

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5
Q

What coordinates vomiting in the brain

A

Vomiting centre in the medulla oblongata of brain stem

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6
Q

What frequently preceedes vomiting

A

Salivation, increase in heart rate, sweating, nausea

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7
Q

Events in vomiting

A

Suspension of intestinal slow wave activity, retrograde contractions from ileum to stomach, suspension of breathing, relaxation of lower oesophageal sphincter, abdominal muscles and diaphragm contract, gastric contents ejected through upper oesophageal sphincter

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8
Q

Why does the glottis close during vomiting

A

To prevent accidental aspiration

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9
Q

Common causes of vomiting

A

Absorbed toxic material and drugs in blood, mechanical stimuli, vestibular system (motion sickness), stimuli within CNS (pain, repulsive sites, fear)

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10
Q

What part of the medulla controls vomiting

A

Chemoreceptor trigger zone (CTZ) in the area postrema and nucleus tractus solitarius

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11
Q

Pharyngeal stimulation, gastric/duodenal distention or irritation goes to the medulla via?

A

Nucleus tractus solitarius

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12
Q

Endogenous toxins ,drugs, vagal afferents stimulate via

A

Chemoreceptor trigger zone (CTZ) that lacks a blood brain barrier

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13
Q

What do enterochromaffin cells in mucosa release to cause depolarization of sensory afferent terminals

A

5-HT or serotonin

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14
Q

Motor output of vomiting is co-ordinated by

A

Group of interconnected neurones within medulla that receives input from nucleus tractus solitarius

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15
Q

Why do sphincters of anus and bladder constrict during emesis

A

To prevent accidental defecation and micturition

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16
Q

Consequences of severe vomiting

A

Dehydration, hypochloraemic metabolic alkalosis raising blood pH, hypokalaemia, Mallory-Weiss tear, aspiration of vomitus

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17
Q

What are prokinetic drugs

A

Increase GI tract motility and lower oesophageal sphincter tone. Ex: Domperidone and Metoclopramide

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18
Q

When do motion sickness H1 antihistamine drugs best

A

When taken 1-2 hours prior to the journey

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19
Q

Additional effect of cinnarizine

A

In addition to it’s H1 antihistamine effect, it has an additional antivertigo effect inhibiting calcium influx, helping tinnitus and Meniere disease

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20
Q

Triple drug regime for chemotherapy induced nausea and vomiting (CINV)

A

5-HT3 receptor antagonist + Dexamethasone (corticosteroid) + Aprepitant (substance P antagonist)

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21
Q

What are NK1 receptors for

A

Substance P

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22
Q

What does the chemoreceptor trigger zone stimulate

A

CTZ stimulates vomiting center in the medulla

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23
Q

What causes pregnancy associated nausea and vomiting

A

Human chorionic gonadotropin (HCG) produced by placenta

24
Q

Non pharmacological treatment of pregnancy associated nausea and vomiting

A

Change in diet, use of ginger or pyridoxine (B6)

Wrist (P6) acupressure

25
What is hyperemesis gravidarum
Excessive vomiting, nausea, weight loss and dehydration during pregnancy
26
Can laxatives/purgatives be used when there is physical obstruction of bowels
No
27
How do laxatives work
Increase peristalsis, soften faeces, cause and/or assist evcuation
28
Misuse of laxatives
Resorted to very early by individuals wanting "regularity". This can cause atonic colon. Also abused in eating disorders
29
When are laxatives indicated
Constipation straining is potentially harmful such as in angina patients or those with haemorrhoids To clear bowel before surgery, endoscopy Treat drug-induced constipation or constipation in bedridden or elderly patients
30
Types of laxatives
Bulk laxatives, osmotic laxatives, stimulant purgatives, faecal softners
31
Mechanism of bulk laxatives
They are indigestible polysaccharide polymers such as methylcellulose (oral). They absorb liquid in the intestine and swell to form a soft, bulky stool. This stimulates the bowel to undergo peristalsis. Acts slow
32
Mechanism of osmotic laxatives
Contain poorly absorbed solutes such as magnesium sulphate or hydroxide (oral), sodium citrate (rectal) and lactulose (oral). These act rapidly by increasing amout of water secreted within intestine forming a softer, easier to pass stool
33
Mechanism of stimulant purgatives
Contain bisacodyl (oral or suppository), sodium picosulfate, senna (anthraquinone laxative) that induce bowel movement by acting to speed up colonic movement (motility)
34
Which laxatives are commonly associated with abdominal cramps
Stimulant purgatives
35
How do faecal softners work
Have a detergent like action that works by increasing amount of water the stool absorbs in the gut, making the stool softer and easier to pass. Docusate sodium (oral), arachis oil (enema), liquid parafin (oral, in the past)
36
What is irritable bowel syndrome (IBS)
Bouts of diarrhoea, constipation or abdominal pain
37
Treatment of irritable bowel syndrome
Treatment is symptomatic with adjustment of diet and anti-diarrhoeals, anti-spasmodics
38
Why can't glucocorticosteroids be used for maintenance inflammatory bowel disease threapy
Prednisolone (oral) and Budesonide (ICS) can be used for acute attack but prolonged use is limited by adrenal suppression
39
What is used for maintenance and mild inflammatory bowel disease (IBD)
Aminosalicylates, generally release 5-aminosalicylic acid (5-ASA) linked to sulfapyridine (associated with adverse effects)
40
Examples of aminosalicylates
Sulfasalazine, mesalazine, olsalazine, balsalazide
41
Aminosalicylates are most effective in what type of IBD
Ulcerative colitis as most aminosalicylate yield 5-aminosalicylic (5-ASA) acid in the colon
42
NSAIDS on kidney function in liver cirrhosis
NSAIDs can worsen hepatorenal syndrome by blocking prostaglandin synthesis in the kidney, PGE is often produced by the kidney to oppose the vasoconstriction
43
What is hepatorenal syndrome
Rapid deterioration in kidney function due to liver failure/cirrhosis. It is due to change in blood flow rather than direct damage to the kidney. This is due to via excess aldosterone release, endothelin release, renal vasocontriction and increased sodium/water retention.
44
Paracetamol toxicity mediation
Paracetamol is metabolized at a constant rate. 8% is metabolized into N-acetyl-p-Benzoquinonimine, a highly reactive intermediate. Glutathione acts on this to convert it into cysteine and mercapturic acid conjugates which can be safely excreted. However, in excess paracetamol, not enough Glutathione is present to metabolise the harmful products. This causes toxicity
45
Paracetamol in liver disease
Glutathione stores are reduced in liver disease. Hence, paracetamol has a longer half life and can cause increased toxicity with normal dose
46
Most common drug induced liver disease
Amoxicillin and Clavulanic Acid induced hepatitis
47
Drug induced liver injury (DILI) pathogenesis
Generalized as a mechanism of direct hepatotoxic effects or idiosyncratic hepatotoxic effects.
48
What is direct drug induced liver injury (DILI)
The direct hepatotoxicity of drugs refers to the direct injury to the liver caused by the ingested drugs and/or their metabolic products.
49
What is Hy's rule
A rule of thumb that a patient is at high risk of DILI if given a medication that causes hepatocellular injury with jaundice
50
Criteria for Hy's rule
ALT/AST > 5 * Upper limit of normal | and Bilirubin > 3 mg/dl
51
Diuretic of choice in liver failure for ascites
Spironolactone as others such as Furosemide (loop) and Thiazide cause hypo-kalaemia and magnesaemia
52
What drugs can be used for sedation
Phase 2 metabolized benzodiazepines such as Lorazepam, Oxazepam, Lormetazepam
53
Side effects of quinolones
Epileptogenic
54
Side effect of Metronidazole
Reduce metabolism
55
Side effects of aminoglycosides
Nephrotoxic
56
What excretion method is preferred for liver drugs
Renal excretion

GI (32 decks)

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