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Pharmacology > Analgesia > Flashcards

Analgesia Flashcards

1
Q

Hydrocortisone

A

Duration < 12 hr
Potency = 1
Uses: topical for pruritis and inflammation assoc. w/ allergy

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2
Q

Fludrocortisone

A

Duration < 12 hr
Potency = 10 (anti-inflam)
Mineralocorticoid potency: 125
Uses: systemically for cortisol and aldosterone replacement during adrenal insufficiency (hypoadrenocorticism/Addisons)

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3
Q

Prednisone

A

Duration 12-36 hrs
Potency = 4
Uses: systemically for long term management of allergy, chronic inflammation (arthritis) and immunosupression (autoimmune disease)
Pro-drug

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4
Q

Methylprednisolone

A

Duration 12-36 hrs
Potency = 5
Uses: systemically for long term management of allergy, chronic inflammation (arthritis) and immunosupression (autoimmune disease)
Used in situations of less prednisone to prednisolone conversion in the body: cats/horses and in hepatic failure

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5
Q

Dexamethasone

A

Duration 36-72 hrs
Potency = 25 (HIGH)
Uses: Systemically for immediate relief of hypersensitivity and septic shock, long term control of allergy and immunosuppression. Best for acute.

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6
Q

Nociceptors

A

Neurons that respond directly to noxious stimuli by starting APs that go directly to the CNS
(Heat cold, pain, chemical)
1st part of the perception of pain
A delta and C fibers

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7
Q

What are Transient Receptor Potential Channels?

A

Peripheral nociceptors activated by heat, pressure, cold, etc and inflammation, which increases pain.

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8
Q

What are some methods of central pain inhibition?

A

Glutamate (NDMA) antagonists -ketamine
Inhibitory interneuron

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9
Q

How do NSAIDs work?

A

Decrease prostaglandin synthesis and TPR activation through COX inhibition.

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10
Q

How do local anesthetics work?

A

Block action potentials, work anywhere along pain pathways.

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11
Q

What is an example of a glutamate antagonist?

A

Ketamine (NMDA)

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12
Q

How do alpha 2 agonists work to limit pain?

A

Work postsynaptically on nonadrenergic neurons

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13
Q

What are two classes of corticosteroids?

A

-Endogenous steroids produced in the adrenal cortex
Cortisol: glucocorticoid (zona fasciculata)
Aldosterone: mineralocorticoid (zona glomerulosa)

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14
Q

Do glucocorticoid drugs often possess mineralocorticoid activity?

A

Yes

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15
Q

Where does corticotrophin releasing hormone come from and what does it do?

A

The hypothalamus
CRH stimulates the anterior pituitary to release adrenocorticotropic hormone (ACTH)

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16
Q

Why is tapering steroids important?

A

High levels of glucocorticoids suppress the production of CRH and ACTH.

17
Q

What are the two basic mechanisms of glucocorticoid signaling?

A

Genomic effects and non-genomic effects

18
Q

Which is faster: genomic or non-genomic signaling?

A

Genomic: slow changes in gene expression that alter cellular function
Non-genomic: rapid changes in cellular function that do not involve changes in gene expression

19
Q

How to glucocorticoids affect metabolism?

A

Increase gluconeogenesis leading to hyperglycemia
Increase insulin secretion and insulin resistance (diabetes mellitus)
Increase protein breakdown
Increase lypolysis and redistribution of lipids (weight gain)

20
Q

How do glucocorticoids affect the heart?

A

Increase vasoconstriction and cardiac contraction
Increase adrenergic signaling
Increase angiotensin signaling
Assoc. w/ hypertension (dogs) and CHF (cats)
Mineralocorticoid effects (NaCl/H2O retention, incr. plasma vol)

21
Q

How do glucocorticoids affect respiration?

A

Bronchodilation
Decrease retention of mast cells in lungs
Decrease histamine release

22
Q

How do glucocorticoids affect skeletal muscle?

A

Muscle wasting (at pharmacological levels)

23
Q

How do glucocorticoids affect the skin?

A

Epidermal and dermal thinning
Easy bruising and poor wound healing
Poor quality hair, alopecia

24
Q

How do glucocorticoids affect the immune system?

A

too little or too much = decreased immune function and increased susceptibility to infection.

25
Q

How do glucocorticoids affect water and electrolyte balance?

A

inhibit ADH release
PU/PD

26
Q

How do glucocorticoids affect the GI?

A

Increased acid and pepsin production
Possible ulceration (esp w/ NSAIDs)

27
Q

Are glucocorticoids anti-inflammatory?

A

At pharmacological/high doses

28
Q

Do steroids help cure the disease?

A

No, steroids help treat the symptoms but do not address the underlying cause.

29
Q

Do glucocorticoids affect cell mediated or humoral immunity?

A

Cell-mediated immunity is suppressed more than humoral.

30
Q

How do glucocorticoids work in inflammation?

A

Suppressed production of inflammatory mediators.
White blood cell migration and function is suppressed
Cell mediated immunity

31
Q

What is iatrogenic hypoadrenocorticism?

A

Induced Addisons from long term steroid administration that is stopped rapidly. Wash out period is important (1-2 weeks)
Additional GC supplementation may be necessary during periods of stress (surgery, anesthesia, illness)

32
Q

Mitotane

A

Adrenal steroid inhibitor
Cytotoxic to zona fasciculata, reduces all adrenal steroids (except aldosterone)
Uses: HyPERadrenocorticism (Cushing’s), steroid-secreting adrenal tumors

33
Q

Cushing’s Syndrome

A

Hyperadrenocorticism
Cats/dogs: hair loss, bald patches
Horses: heavy haircoat that does not shed

34
Q

COX 1

A

Constitutive expression
-Involved in homeostatic processes
-Gastric mucosal protection, renal function, vascular function, and platelet function
Produces:
-PGE2 (prostaglandin E2) : vasodilation, sens of nociceptors, GI protection
-TxA2 (thromboxane A2): platelet aggregation and vasoconstriction > enhanced coagulation and clot formation

35
Q

COX 2

A

inducible expresion
-expressed at site of injury and inflammation
Produces:
PGE2
PGI2 (prostacyclin): vasodilation, inhibits platelet aggregation
in the kidney these alter blood flow, stimulate renin, increase Na excretion, decr. Na absorption

36
Q

What is the most common side effect of COX 1/2 inhibition?

A

GI related effects

37
Q

What is an advantage of COX-2 selective drugs (COXIBs)?

A

Less GI effects

Pharmacology (17 decks)

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