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Gastro block > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Give an example of a proton pump inhibitor. what does this treat?

A

Omeprazole. Inhibits the H+/K+ ATPase in parietal cells and thus blocks all acid secretion into lumen.
Treats severe gastric ulcers

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2
Q

Give an example of a H2R antagonist. what does this treat?

A

Ranitidine. Prevents histamine-mediated acid secretion from parietal cells.

Treats mild cases of gastric ulcers. Few side effects, avail over the counter

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3
Q

What is Sucralfate used to treat? What is it?

A

It is cytoprotective: protects the ulcer site from acid in peptic ulcer disease

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4
Q

Give an example of an antacid. What do these do?

Limitations?

A

Magnesium hydroxide and sodium bicarbonate
Neutralise stomach acid rather than stopping its secretion.

You have to give a lot all the time, because it is short acting and increases the luminal pH which stimulates gastrin to release MORE acid.

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5
Q

Why didn’t PGE analogues work in the treatment of peptic ulcers?

A

Diarrhoea and spasm and abortion as side effects

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6
Q

What is a spasmolytics, how does it work and what does it treat?
Give 2 examples

A

Smooth muscle relaxant, reduces spasm and slows down movement of the gut.

Musc R antagonists = Hyoscine Butylbromide
Direct spasmolytics are idiosyncratic: Peppermint oil

Treat IBS, PUD, gut spasm

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7
Q

Side effects of Hyoscine Butylbromide

A

It is a muscarinic R antagonist used to reduce gut spasm. Side effects are anti-SLUD (dry mouth, urinary retention, constipation)

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8
Q

What 2 centres in the brain are involved in vomiting and how do they relate to one another?

A
  1. Vomiting Centre: in medulla, receives afferents from many diff places including CTZ and inner ear
  2. Chemoreceptor Trigger Zone: in medulla but outside BBB so can respond to circulating toxins, drugs, bacteria; feeds into VC
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9
Q

What receptors are involved in vomiting?

A

DA D2R and 5HT3R: CTZ

H1R and AchR: VOMITING CENTRE, involved in motion sickness and inner-ear type

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10
Q

Give an example of a muscarinic receptor antagonist used as an anti-emetic. What else is it used for in the gut?
Draw-backs?

A

Hydroscine hydrobromide. Also used as a spasmolytic to decr gut motility.
Anti-SLUD side-effects and drowsiness

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11
Q

Give an example of an antihistamine used as an anti-emetic. Which receptor does it target?
What else is it used to treat

A

Promethazine. Targets H1R.

Also treats allergies and as a sedative

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12
Q

Metaclopramide - what does it treat and where/how does it act?

A

Anti-emetic (prevents nausea and vomiting triggered via CTZ) and gastro prokinetic (Speeds up gastric empyting) - note that nausea is caused by gastric stasis

D2R antagonist, also HT3 antagonist and HT4R antagonist

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13
Q

Give 2 examples of D2R antagonists used as anti-emetics.

What are possible side-effects and why do these occur? How would you limit these?

A

Metaclopramide
Prochlorperazine

Side effects are extra-pyramidal: Parkinsons like dystonias and dyskinesias (decr voluntary/incr involuntary movements) because drugs can cross teh BBB and enter CNS.
Limit dose by combining w 5HT3R antagonist

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14
Q

What are the various uses of D2R antagonists?

A

Anti-emetics
Prokinetic in gut
Anti-psychotics

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15
Q

Ondansetron. What does it treat and how?

A

Anti-emetic drug - relieve nausea and vomiting associated w cytotoxic drugs
5HT3R antagonist

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16
Q

Ondansetron. what is it? side effects?

A

Anti-emetic. Constipation and headache

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17
Q

Possible causes of constipation

A 
Inadequate dietary fibre
Inadequate fluids
Poor bowel habits
Inadequate physical activity
Drugs (opiods, antacids, anticholinergics)
Dementia
Depression
Bowel obstruction
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18
Q

Diff types of laxatives (4)

A
  1. Bulking agents
  2. Faecal softeners and lubricants
  3. Osmotic laxatives
  4. Irritant laxatives
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19
Q

Give 2 examples of bulking agents. What do they treat and how?

A

Psyllium
Bran
Treat constipation - ingested w water, swell with water and make bulk which activates stretch receptors and stimulates normal peristaltic activity

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20
Q

Bulking agents: contraindications and side-effects

A

Contraindicated w people taking opiods (slows bowel movements)
Side-effects: esophageal congestion if they are taken toos lowly and swell before reaching gut; flatulence

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21
Q

Give an example of a faecal softener/lubricant. When is it used and how does it act?

A

Docusate.

Laxative prescribed w opiods to lessen their constipative side-effects
Detergent - emulsifies fat to soften faeces.

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22
Q

Give an example of an osmotic laxative. How does it work?

A 
Magnesium Sulfate (Epsom salts): 
Osmotic  laxatives are non-absorbable osmotic substances that attract and retain water in the intestinal lumen -> incr fluid vol in lumen stimulates bowel evacuation via distention -> activation of mechanical stretch receptors
23
Q

What do you need to be careful about with osmotic laxatives?

A

Wary of fluid and electrolyte loss

24
Q

Irritant laxatives: give an example. how do they work?

A

Senna
Irritates intestinal mucosa -> activate sensory nerves directly OR stimulate colonic myenteric nerve plexus -> increase motility

25
Irritant laxative: what do you need to be careful of?
Loss of water and electrolytes and decreased net absorption due to increased motility of gut. DEHYDRATION
26
Xenograft
organ from one species to another
27
Autograft
Tissue from one part of body to another
28
Isograft
Organ from twin (genetically identical)
29
Allograft
Transplant between members of same species
30
What process causes skin graft/transplant rejection?
Immune response against foreign Ag (donor's tissues) Skin grafts between 2 allogenic individuals rejected in predictable manner re timing and magnitude. Second skin graft from same donor to same recipient shows accelerated rejection due to stronger immune response (memory and specificity)
31
What immune cell and molecules are primarily responsible for graft rejection and how?
T cells and MHC molecules (Ag presentation to T cell) CD8 - MHCI (present on all cells) CD4-MHCII
32
How are recipients determined to receive renal transplants? how does this differ from other transplants?
Determined by degree of HLA (MHC) matching between donor and recipient. Each mismatch decreases the chance of transplant success. Kidneys can be preserved on ice (not time critical) and there is a national registry for HLA matching of patients waiting for transplant. All other transplants don't have this - accept whatever form of mismatch comes along because no national registry and more time critical.
33
Hyperacute/Ab mediated /humoral immune rejection
Can occur min after transplant. Due to pre-formed Ab. Alloantigen (HLAmismatch OR putting wrong blood into someone) is recognised by alloantigen-specific antigen Ab (ex: pre-formed Ab against wrong blood group) mount immune response against the foreign RBC/tissue -> C' cascade -> inflame -> damaged, dead allograft
34
Acute allograft rejection
1wk-3mo post transplant usually Highly vascularised organs show earliest signs. Due to development of cellular (Tcell-mediated) immunity Diagnosis via H&E stain -> presence of lymphocytes and monocytes in tissue, causing damage.
35
Chronic allograft rejection
Long-term accumulation of damage to transplanted organs -> leads to fibrosis of tissue blood vessels Due to humoral and cellular injury, viruses, ischaemia-reperfusion injury Morbidity of transplant organ ~4.7 years Symptoms depend on organ affected: Kidney -> fibrose tubules -> renal failure Liver -> fibrosed bile ducts -> jaundice Lung -> fibrosed bronchioles -> cough, airflow obstruction heart -> fibroseD CA -> angina
36
Ways to prevent transplant rejection
``` Get rid of harmful antibodies Match MHC alleles (identical twins) Combined use of immunosuppresive drugs: inhibit the T cell! (top of hierarchy): Corticosteroids (prednisolone) Cyclosporin Anti proliferative drugs (azathioprine) ```
37
Cyclosporin
Decr gene transcription of Il2; selectively inhibits recently activated T cells Used to prevent transplant rejection Side-effects: latent viruses become active (HSV, EBV EMV etc) Nephrotoxicity
38
Azathioprine
Anti proliferative drug, inhibits DNA and RNA synthesis -> inhibits proliferation of rapidly dividing cells Used to prevent transplant rejection Side effects: Nausea (inhibits profile of rapidly dividing enterocytes in GIT)
39
Top 3 transplant organs
1. Renal 2. Lung 3. Heart
40
Future possibilities for better transplant success
1. Better immunological matching of host and recipient 2. More specific immunosupression 3. Xenotransplantion (pigs?) 4. Stem cell transplants (heart-muscle) 5. Bone marrow transplant w organ to induce tolerance to transplant 6. Organ regentation: decellularise donor's organ and recellularise w recipient's damaged cells
41
Hypersensitivity type II | 2 possible response outcomes
Ab bind to HOST Ag -> C' activation: chemotaxis, opsonisation, membrane attach complex formation (Inflammation) 1. Tissue damage due to inflammatory process 2. Abnormal physiological response: Ab bind to receptors-> over activation or under activation of receptor, interfering with function
42
Examples of T2HS reactions
1. Blood group antigens 2. Penicillin allergy 3. Haemolytic disease of newborn 4. Goodpasture's syndrome 5. Grave's disease 6. Myasthaenia gravis
43
Haemolytic disease of newborn
T2HS Mother who is Rh- has second child who is Rh+ (from father) - in first pregnancy, Rh Ag crossed over placenta into mother's blood stream and mum made Rh-antibodies. With second pregnancy, mother's Rh-Ab (isotope switching and affinity maturation has occurred) cross placenta into foetus and C' fixation lyses RBCs Baby is born anaemic.
44
Penicillin allergy:
T2HS Penicillin binds to RBCs, rendering the RBC a target for antibodies -> antibodies bind the drug-RBC complex -> complex is phagocytosed by splenic macrophages -> anaemia or thrombocytopenia
45
Blood group antigens
T2HS Giving the wrong type of blood to someone who has antibodies against that blood type leads to RBC lysis due to C' fixation -> Shock, death
46
Goodpasture's syndrome
T2HS (Note: normally TSH released from pituitary which activates TSHR in thyroid -> production of thyroid hormones which feedback to inhibit TSH release - control!) In Goodpasture's, antibodies against TSH R activate that receptor and stimulate thyroid hormone production. Thyroid hormone produced feeds back to inhibit TSH release from pituitary gland whilst continually activating the TSHR. Control is lost! Result is hyperthyroidism.
47
Myasthenia Gravis
Antibodies against AchR at neuromuscular junction bind to AchR and inhibit Ach binding -> internalisation and degradation of receptors. Result is muscle wasting, ultimately leading to resp failure and death
48
Type III HS reactions
Build up of Ab-Ag complexes (IgG or IgM mediated) due to 1. too many immune complexes overwhelm immune system 2. ineffective clearing of immune complexes
49
Why do immune complexes persist in circulation rather than being cleared?
Smaller complexes are cleared more inefficently Ag in excess/too few Ab Low affinity Ab (poor complex formation) Inefficient C' activation
50
How are immune complexes normally cleared by the immune system?
Ab binds R -> cross-linking of Ab-Ag binding forms complexes -> C' fixation -> c3b deposited on surface of immune complexes -> RBCs expressing C3bR bind C3b on complexes ->Resident macrophages remove RBCs with Ag-Ab complexes attached to spleen
51
What happens when immune complexes aren't cleared effectively? How does this present?
Fave time to build up and deposit -> ionic binding in basement membranes!! Especially in vessels - primary form in organs w dense capillary networks (kidney, liver etc) Build up over time; once you reach threshold complex [] to activate enough C3b, C' etc, you get C' activation Presentation depends on WHERE complex deposits Vasculitis (low pressure capillary walls) Arthritis (joints) Chronic hepatitis (kidney) Rheumatic fever and endocarditis (heart)
52
3 broad categories of diseases resulting from T2HS reactions (immune complex deposition) + specific examples of each
Persistent infection by microbial antigen, in infected organs or kidney (generally in immunocompromised patients-HIV) -> Chronic hep (liver) and chronic renal disease (kidneys) Autoimmune diseases against self-antigens (Systemic lupus erythematosis (often causes immune complex deposition in glomerulus of kidneys -> glomerular nephritis; also in skin causing rash) Inhaled antigens (from mould, plant, animals complex w Ab in lung alveoli -> inflammation and fibrosis in lungs (farmer's lung)
53
Central tolerance vs peripheral tolerance
Central tolerance: removal of self reactive lymphocytes from primary lymphoid organs in development, before they are able to escape into periphery Peripheral tolerance: other mechanisms in periphery ensure auto reactive cells that pass initial screening aren't activated (control of self-reactive lymphocytes)

Gastro block (6 decks)

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