Test 1 Flashcards

(24 cards)

1
Q

What are the characteristics of glucocorticoids?

A
  • Glucocoritocids are secreted from ADRENAL CORTEX, which is stim from ACTH from the hypophysis (HF), which is then stim from CRF from hypothalamus (HT)
  • Gcc can go through membrane, to the glucocorticoid receptor in the cytoplasm.
  • > Together they can enter the nucleus of the cell (to impact the genes)
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2
Q

Physiological effects of Glucocorticoids

A
  • It’s a stress hormone - mobilizing hormone
  • Inhibits the effect of insulin (antagonist of insulin)
  • Stimulate gluconeogenesis (in liver) from proteins and fats
  • Ketone bodies produced
  • Decrease cellular glucose use -> muscle weakness
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3
Q

Pathological effect of Glucocorticoids

A
  • Muscle weakness, atrophy
  • Osteoporosis (bc decreased calcium absorption)
  • Delayed wound healing (bc decreased collagen synthesis)
  • Alpoecia and thinning of skin
  • Decrease growth
  • PU/PD
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4
Q

Pharmacological effect of Glucocorticoids

A
  • Antiallergic
  • Antiinflammatory
  • Antishock
  • Immunosuppressive
  • Neuroprotective
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5
Q

Mechanism of action of Glucocorticoids

A

(Cellular damage - membrane phosphorlipids - (By phospholipase A2) - arachidonic acid - (by COX) - PG)

Gcc inhibits PLA2

Antiinflammatory and immunosupressive effects:

  • Inhibit PLA2 (Membr. phosphorlipids converting to arachidonic acid, which convert to prostagladins etc)
  • COX enzyme expression decreases (which prod. prostagladins)
  • Inhib. expression of interleukins (IL-1, IL-2, 3, 4, 5, 6, 10, 12)
  • TNF and IFN synth. decreased
  • Apoptosis
  • Neutrophilia

Antishock:

  • Vasoconstiction
  • Decrease membrane permeability (enhance microcirculation)

Neuroprotective:
- Trauma will lead to bleeding, which will lead to vasoconstriction
- Ischemia can lead to lipid peroxidation -> ROS released -> apoptosis and necrosis!
However, Gcc will inhibit lipid peroxidation and enhance microcirculation

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6
Q

Active substances (+ effect) of Glucocorticoids

A
  • Cortisol (short)
  • Prenisolone (medium)
  • Methylprednisolone (medium)
  • Betamethasone (long)
  • Dexamethasone (Long)
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7
Q

Side effects of Glucocorticoids

A
  • HT - HP - adrenal cortex axis inhibition
  • Gastric ulcers (inhib. PG) - treat with omeprazol - gastroprotective)
  • Hepatopathy (ALKP increase sign.) - treat with silimarine - hepatoprotective
  • Pancreatitis
  • Thinning of skin, delayed wound healing, alpoecia
  • PU/PD
  • Polyphagia
  • Glaucoma/cataracta
  • Muscle atrophy
  • Immunosupression
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8
Q

Systemic usage and indications of Glucocorticoids

A

Systemic usage:

1) High dosage, once (e.g. omeprazole)
- short term, few side effects
2) ADT (alternate day therapy) (e.g. prednisolone, methylprednisolone)
- every other day (mornings for dogs and evenings for cats)
3) Long acting injections (depot)
- not recommended
- only if tablet can not be administered

Indications:

1) Local use (atropic dermatitis)
2) Single injectable dose
3) Inhalation usage (asthma, RAO)
4) Intraarticular
5) ADT
6) Depot injections

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9
Q

Indications of immunosupression

A

1) Autoimmune diseases
- lupus, IHA, KCS
2) Hypersensitivity diseases
- Atopic dermatitis, asthma, RAO, Inflammatory bowel disease
3) Transplantation
- Need to supress the immune system to accept new organs if transportation

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10
Q

Immunosupression drugs:

- Antimetabolites

A
  • Purine-analogues:
    azathioprine (for autoimmune diseases)
  • Pyrimidine- analouges:
    Leflunomide (rheumatoid arthritis and psoriatic arthritis)
  • Folic acid antagonists:
    Methotrexate (antineoplastic)
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11
Q

Immunosupression drugs:

- Alkylating agents

A

Cyclophospamide (antineoplastic and autoimmune disorder)

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12
Q

Immunosupression drugs:

- Glucocorticoids

A
  • Cortisol
  • Prednisolone
  • Methylprednisolone
  • Betamethasole
  • Dexamathasole
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13
Q

Immunosupression drugs:

- Cytokine gene expression inhibitors

A
  • Cyclosporin: Autoimmune diseases, atopic dermatitis, IBD
  • Tacrolimus: more active than cyclosporin, but more toxic! For atopic dermatitis
  • Pimecrolimus: more active than cyclosporin, but more toxic! Locally atopic dermatitis, KCS
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14
Q

COX enzymes; function, Location, Constitutive/ induced,

A

COX- enzymes helps the production of prostagladins and Thromboxane.

COX- 1: physiologic! Located in stomach, kidney and platelets. Always present (constitutive) and is a good enzyme to maintain hemostasis.

Stomach: COX1 are physiologic, and prevents too much acid to be prod. If COX are inhibited too much acid will be produced.

Kidney: COX1 are physiologic, helps maintain normal flow to kidneys (vasodilation). If inhibited kidney will not remain normal flow and kidney will be damaged.

Platelets: COX1 physiologic. Produces thromboxane, so platelets can aggregate in case of trauma. If inhibited longer bleeding time. (So NSAIDs which inhib. COX can be good for thrombotic patients).

COX- 2: is only present during inflammation. Located at macrophages and fibroblasts. Induced during inflammation.

COX- 3: in brain (HT)
For sensation of fever and pain.
Inhib. by paracetamol (analgestic) and methamizole (antipyretic, analgestic) .

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15
Q

COX selectivity

A

We want drugs with higher affinity to COX-2, since that is the inflammatory enzyme. High COX2:COX1 ratio is good.

Firocoxib (Very selective: safest) 
Deracoxib
Carprofen
Meloxicam 
Ketoprofen
Aspirin (Not selective)
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16
Q

Pharmacological effects of NSAIDs

A
  • Antiinflammatory
  • Antiendotoxin
  • Antipyretic
  • Antineoplastic
  • Spasmolytic
  • Platelet aggregation inhibition
  • Analgestic
17
Q

Phatmacokinetics (er dette viktig tho) of NSAIDs

A

Absorption: weak acids

Distribution: Extensive albumin binding (Hypoalbuminemia is a consequence)

  • Interactions: Don’t combine with other drugs that bind to albumin
  • WP: short or no wp in milk.

Metabolism: Mostly glucuronic acid conjugation -> feline sensitivity

Excretion: urine active + inactive

18
Q

Side effects of NSAIDs:

A
  • GI ulcers (treat with omeprazole)
  • Kidney damage
  • Platelet aggregation inhibition (aspirin and ketoprofen)
  • Hepatotoxicity (Paracetamol and carprofen)
  • Allergic reaction
  • Methaemoglobinemia (paracetamol in cats)
  • Fetal damage
  • Placental retention
  • Cardiotoxicity
  • Cartilage damage (bc aspirin and ketoprofen)
19
Q

NSAIDs drugs:

A

1) Aspirin (Dog and farm animals)
can cause:
- Platelet aggregation inhibition
- cartilage damage

2) Ketoprofen
can cause:
- Platelet aggregation inhibition
- cartilage damage

3) Carprofen
can cause:
- hepatotoxicity

4) Meloxicam - Safe in cats!!
- It’s antiendotoxin

5) Deracoxib (dog)
- COX2 selective
6) Firocoxib (dog and horse)
- COX2 selective

and

Etodolac: Safe

Flunixin
can cause:
- Platelet aggregation inhibition
- Antiendotoxic

Paracetamol: NEVER to cats
- COX-3 inhibitor: analgesic, antipyretic (minor analgesic)

can cause:

  • Hepatotoxic
  • Methaemoglobinaemia (cat)
20
Q

JAK- inhibitors indications

A

1) Rheumatoid arthritis
2) Crohn disease
3) Leukemias
4) Alopecia

21
Q

JAK- inhibitors action

A

Cytokine binds to cytokine receptors. There will be a phosphorylation of receptors, then STAT will bind to both sides of the receptors. The phosphorylated STAT will go through the nuclear membrane and bind to DNA

22
Q

JAK- inhibitors drugs: 1

  • Indication
  • Inhibition
  • Pharmacological effects
  • Pharmacokinetics
  • Side-effects
A
  1. Oclacitinib:

Indication: Itching and atopic dermatitis

Inhibits: mainly JAK-1,
IL-2, 4, 6, 13 (allergy and inflam.)
and IL 31 (pruritus)

Pharmacological effects: Antiinflammatory, antiallergic and antipruritus

Pharmacokinetics: Per Os, with food.

  • Metabolism in liver
  • Can be given with other drugs

Side-effects:
WBC decreased, Cholesterol increased, vomiting and diarrhoea

23
Q

JAK- inhibitors drugs: 2

  • Indication
  • Inhibition
  • Pharmacological effects
  • Pharmacokinetics
  • Side-effects
A
  1. Lokivetmab

Indication: itching

Inhibition: IL- 31

Pharmacological effects: Antiinflammatory, antiallergic and antipruritus???

Pharmacokinetics: Once a month, SC

Side-effects: Anaphylactic shock and allergic reaction

24
Q

Classes of antihistamine:

A
1st generation:
 Prometazine
 Hydroxyzine
 Chloropyramin
 (mangler et par her tho)

2nd generation:
Lorataadine,
cetirizine,
levocetirizine