Lecture 4 Flashcards
List some immunosuppressive agents
immunosupressive agents
- antithymocyte ab
- monoclonal ab
- soluble receptor fragments
- drugs like cyclonsporine and azathioprine steroids
For immunosuppressive drugs discuss glucocorticoids
Immunosuppressive drugs
glucocorticoids- endogenous glucocorticoids have a very strong immunosuppression response
glucocorticoids role in the body is to reduces certain aspects of immune function, such as inflammation. They are therefore used in medicine to treat diseases caused by an overactive immune system, such as allergies
what glucocorticoids does in the body will be highen when you add it has a drug
corticosteroids e.g prednisolone
List the different types of immunosuppressive drugs and list the examples and how they work
Immunosuppressive drugs
these drugs are corticosteroids like prednisolone is your 1st line
-immunophilin binding drugs;
calcineurin inhibitors
cyclosporine
-cell division (stops it) and nucleotide metabolism inhibitors
drugs will target cell division because it will be occurring very fast and therefore this will be very effective for immunosuppression and this may also effect organs which have high cell division as well
examples are;
azathioprine
cyclophosphaminde
-JAK-STAT signalling inhibitors
oclacitnib targets destruction via cytokines
-others eg. danazol (down regulates fc-receptors)
For glucocorticoids list the effects on the body
what to watch out for
dose level
what do they destroy
stabilising cell membranes (what do they inhibit)
antagonise an increase in blood flow (how does this occur)
lympholytic (what is inhibited/ decreased)
Glucocorticoids
-what to watch out for; anti-inflammation and immunosuppressive effect
must be careful when treating bacteria infection with these types of drugs because you don’t want to suppressive the immune system and depending on the
-dose level you can control if the drug targets the immune system of inflammation
-they will destroy T lymphocytes
-stabilising cell membranes
inhibit phospholipases and release of TNF and inhibits the platelet activation factor
-antagonise an increase in the blood flow; causes vasodilation, prevents fibrin deposition, fibroblast proliferation and the formation of collagen
-lympholytic; may decrease circulating lymphocytes, induce impairment of chemotaxis and lysomal enzyme secretion. May also inhibit complement inflammatory pathways
For Corticosteroids explain the MOA
Corticosteroids explain the MOA
at low doses you are effect have anti-inflammatory response and effect the production of arachidonic acid
cortisol drives suppression of the immune system and loss of hair because the the cortisol is destroying the certain cell types
prednisolone will drive these effects
the drug enters the cell into the cytoplasm and binds to the glucocorticoid receptor when it binds its activated and goes into the nucleus of the cell it will activate genes which will either activate and suppression things like the immune system and then you will end up with things like neutrophil migration suppression and depression in production of proinflammatory cytokines like interferon, TNF aphla
For the flowing drugs state the duration of action, potency and salt retention
- Dexamethasone
- Betamethasone
- Prednisone
-Dexamethasone
duration of action; long (greater than 48 hrs)
anti-inflammatory potency; 30 very strong effect because its so potent
-Betamethasone
duration of action; long (greater than 48 hrs)
anti-inflammatory potency; 35 very strong effect because its so potent
-Prednisone
duration of action; intermediate (12-36 hrs)
anti-inflammatory potency; 4
you retain more salt and water which helps with inflammation so with hypertension and anaphylaxis causes a drop in blood pressure and this drug will cause an increase in increase blood pressure because of the water and salt
For Corticosteroids list the adverse effects of prolonged use and what occurs when you go cold turkey
Corticosteroids; adverse effects
can cause cushions in patients
effects of prolonged use may include
fever, myalgia (muscle pain), malaise (discomfort)
fluid and electrolyte imbalance
hypertension
hyperglycaemia, polydipsia (excessive thirst), polyuria (excessive pissing)
increase GIT infections
pituitary adrenal suppression and behavioural
abortions
pancreatitis, osteoporosis and myopathy
MUST COME OFF THE DRUG SLOWLY OR ELSE YOU GET ADDISON’S DISEASE (opposite of cushing) because they body will not produce its own cortisol
List the principle of therapy for corticosteroids
principle of therapy for corticosteroids
you can titrate your doses of corticosteroids to get it to do what you want
-short duration and dingle doses, low conc maybe harmless and effects are very specific
cats are more resistant to immunosuppressive not adrenal suppressive effects
higher doses are required for immune suppression
don’t don’t stop treatment prematurely
List some clinical indications of corticosteroids
clinical indications of corticosteroids
- autoimmune and some neoplastic inflammatory conditions
- adjunct therapy in hypoadrenocorticism
- some cases of asthma and anaphylactic shock
- cutaneous hypersensitivity eg. atopic dermatitis
- immune mediated inflammatory ocular disease
What drug is used as a first line gluocortoid for acute inflammation and immune mediated disease condition for its good efficacy for reducing neutrophil migration, cytokine secretion and T cell mediated cytotoxicity
- Prednisone
- Dexamethasone
In treating lymphoma in dogs, many different chemotherapeutic agents are combined with prednisolone outline 3 adverse effects associated with the prolonged use/ high dose of prednisone
infection because you suppressed the immune system
can get cushion
muscle distrunction
For cyclosporine explain the MOA
cyclosporine explain the MOA
need to deactivate this molecule when it binds
this drives T lymphocyte activate which drives the production of clone explanation of T lymphocytes
use this drug for T mediated cell immunity
in cytosol, cyclosporine enters and inhibits the calcineurin @ specific sites and this stops the activation and entry of nucleus by NFAT which is a transcription activator
