Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HLTH 2511 > Module E > Flashcards

Module E Flashcards

1
Q

List 4 important classes of autocoids

A

Histamine, serotonin, prostaglandins, leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Compare and contrast the locations and functions of H1, H2, and H3 receptors

A

H1: Found throughout the body (CNS, skin, airways). Activation causes alertness (hence drowsiness with antihistamines). Peripheral activation causes hives/rashes, erythema, pruritis, edema, cough, and bronchoconstriction

H2: Found in glandular and smooth muscle tissue of GIT, uterus, and vasculature. Activation causes gastric acid release and smooth muscle relaxation

H3: Autoregulatory inhibitory histamine receptor found throughout the nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Antihistamines ______ (are / are not) effective once an allergic reaction is underway.

A

are not!

they should be used prophylactically to reduce frequency, severity, and duration of allergic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

The major difference between first and second generation antihistamines is:

A

first generation antihistamines cross the blood-brain barrier and cause sedation/hypnosis, second generation antihistamines do not

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The major clinical use of H2 receptor antagonists is:

A

reduce gastric acid production in GERD (ex: Zantac (ranitidine))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Benadryl (Diphenhydramine)

A
  • First-generation antihistamine, H1 receptor antagonist
  • Blocks H1 receptors systemically, including the CNS
  • Used to manage symptoms of allergy, but may cause unwanted sedation/hypnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Allegra (Fexofenadine)

A
  • Second-generation antihistamine, H1 receptor antagonist
  • Blocks peripheral H1 receptors, does not closs blood-brain barrier
  • Alleviates allergy symptoms without causing significant sedation/hypnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Claritin (Loratadine)

A
  • Second-generation antihistamine, H1 receptor antagonist
  • Blocks peripheral H1 receptors, does not closs blood-brain barrier
  • Alleviates allergy symptoms without causing significant sedation/hypnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Zantac (Ranitidine)

A
  • H2-receptor antagonist
  • reduces gastric acid secretion to reduce dyspepsia/gastroenteritis in GERD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Tagamet (Cimetidine)

A
  • H2-receptor antagonist
  • reduces gastric acid secretion to reduce dyspepsia/gastroenteritis in GERD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

3 important endogenous sources of serontonin (5-HT) are:

A

platelets, neurons, GI cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the PNS effects of serotonin

A
  • Platelet aggregation
  • Vasoconstriction
  • Bronchoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the biosynthesis of eicosanoids, list the three main classes, and generally describe their effects

A

Arachidonic acid is cleaved from membrane phospholipids by phospholipase A2 (ex: following injury). This then follows one of two pathways; cyclooxygenase (COX) initiates a metabolic pathway leading to production of prostaglandins and thromboxanes. 5-Lipoxygenase initiates a pathway leading to production of the Leukotrienes. These local hormones have varied and often opposing effects (ex: vasoconstriction and vasodilation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Group the prostaglandins/thromboxanes by vaso/bronchodilating vs. contricting effects

A

PGF, PGD, and TXA2 all cause bronchoconstriction and vasoconstriction

PGE and PGI (prostacyclin) cause bronchodilation and vasodilation

also note that TXA2 causes platelet aggregation, while prostacyclin (PGI) inhibits it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Leukotrienes produce _______ (opposite / similar / greater) effects compared to histamine

A

similar and greater!

leukotrienes are responsible for the late phase reaction in anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Briefly describe the effects of PGE and PGE analogues and how they are used therapeutically

A
  • cause vasodilation, bronchodilation, and smooth muscle contraction in the uterus
  • used to treat PAH and ED, maintain a patent ductus arteriosus, and induce labour.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Briefly outline causes and treatments of PAH

A
  • could be due to NO or PGI deficiency, or overabundance of endothelin-1 (ET1)
  • non-specific treatments include oxygen, diuretics, cardiac glycosides
  • specific therapies include CCBs, PGI (epoprostenol), NO donors, ET1 receptor antagonists, etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Contrast the roles of COX-1 and COX-2 in the body

A

COX-1 is a “housekeeping” enzyme, it is continuously expressed in gastric tissues and promotes mucus production with inhibited gastric acid secretions

COX-2 is an “inducible” enzyme, it is up-regulated in most tissues as a result of tissue injury causing prostaglandin/TXA2 production and inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the role of eicosanoids in inflammation

A

eicosanoids are produced by the COX and 5-lipoxygenase pathways in response to tissue injury. They cause vasodilation, platelet aggregation, chemotaxis, heat production, and increased sensitization of pain receptors

20
Q

Aspirin (ASA)

A
  • NSAID, non-specific COX inhibitor
  • causes irreversible inhibition of platelet COX enzymes. Reduces PG and TXA2 production in a dose-dependent fashion
  • used for anti-inflammation, anti-inflammatory, analgesic, and anti-platelet effects
  • Has an anti-platlet effect which is longer-acting than analgesia
  • Increased risk of GI bleeding, ulcers, can cause tinnitus, respiratory alkalosis, and asthma
  • may potentiate Reye’s syndrome in children with viral infection
21
Q

Contrast the antiplatelet and antiinflammatory actions of aspirin

A

antiplatelet action is provided by irreversible addition of an acetyl group to the active site of COX (the acetyl from ASA)

The remaining salicylate moiety acts as a competitive COX inhibitor providing the inti-inflammatory effects.

22
Q

Motrin/Advil (Ibuprofen)

A
  • NSAID, non-selective COX inhibitor
  • competitively inhibits COX enzymes, reducing PG and TXA2 synthesis in inflammation
  • used to reduce pain, inflammation
  • May cause GI, hepatic, and renal side effects due to COX-1 inhibition
  • does not produce the anti-platelet effects of ASA
23
Q

Celebrex (Celecoxib)

A
  • NSAID, selectie COX-2 inhibitor
  • Reduces PG production associated with inflammation without causing gastric irritation
  • used in management of pain and inflammation
  • increased risk of cardiovascular events (MI, CVA)
24
Q

Tylenol (Acetaminophen)

A
  • Not strictly an NSAID; non-opioid analgesic/antipyretic
  • MOA not udnerstood, but may involve COX-3. Does not affect COX-1 or COX-2
  • reduces pain and fever associated with inflammation
  • No associated GI effects or Reye’s syndrome
  • causes hepatic toxicity in overdose that rapidly escalates with higher doses as toxic metabolites accumulate
25
Q

Compare and contrast non-selective NSAIDs, coxibs, and acetominophen

A
  • Ibuprofen/naproxen: effective anti-inflammatories and analgesics. No anti-platelet effect. cause GI/renal side effects
  • ASA: effective anti-inflammatory and analgesic with anti-platelet effect. Causes GI side effects and increases risks of bleeding.
  • Coxibs: COX-2 selective. Highly effective anti-inflammatories and analgesics without GI side effects. Increased risk of adverse CV events
  • Acetominophen: not an NSAID, MOA unknown. Analgesic and antipyretic. No GI side effects, hepatotoxic in overdose.
26
Q

Describe how exogenous corticosteroids affect the HPA axis

A

hypothalamus recognizes exogenous CS drugs as endogenous and down-regulates CRH production. This leads to decreased ACTH expression and decreased activation of the adrenals. Prolonged use may lead to adrenal hypoplasia

27
Q

Describe the circadian rhythm of corticosteroids

A

Corticosteroids are usually produced mainly during sleep and are at a maximum level in the morning after waking. They gradually decline in concentration during the day, reaching a minmum concentration at midnight.

28
Q

Describe the effects of corticosteroids on glucose metabolism

A

CS drugs increase circulating glucose by inhibiting insulin, promoting glycogenolysis (in muscles), and promoting gluconeogensis. Gluconeogenesis is promoted by increased muscle wasting, freeing amino acids for glucose production.

29
Q

Corticosteroids bind to __________ (intracellular / extracellular) receptors

A

intacellular

glucocorticoids are hydrophobic and cross the plasma membrane freely. They are transported in blood by binding to albumins and globulins.

30
Q

The two major clinical uses of corticosteroids are:

A

anti-inflammation, treatment of adrenal insufficiency (esp. Addisonian crisis)

31
Q

If available, the preferred routes of corticosteroid administration for inflammation are:

A

topical, inhalational

32
Q

Give an example of a short-acting, intermediate-acting, and long-acting corticosteroid

A
  • Short: Hydrocortisone, cortisone (8-12 hrs.)
  • Intermediate: Prednisone (12-36 hrs.)
  • Long: Dexamethasone, Betamethasone (24-72 hrs.)
33
Q

Describe the anti-inflammatory effects of corticosteroids

A
  • broadly inhbiit eicosanoid (PG, TXA, LT) production by producing inhibitory proteins for phospholipase A2. This inhibits release of arachidonic acid.
  • Inhibit production of pro-inflammatory cytokines, reducing eosinophil recruitment and chemotaxis
  • Decrease production and recruitment of inflammatory cells like macrophages, T-lymphocytes, neutrophils, eosinophils, mast cells
  • Decreases histamine synthesis and release by stabilizing mast cell membranes
  • cause constriction of microvasculature
34
Q

If a prolonged regimen of corticosteroids is required, why must the dose be slowly tapered off at the end of treatment?

A

CS drugs disrupt the HPA axis and decrease endogenous CRH, ACTH, and CS production. Dose must be reduced slowly to restore equilibrium and prevent adrenal insufficiency (addisonian) crisis

35
Q

Describe how alternate-day therapy for CS drugs is used

A

for prolonged regimens of high-dose or high-potency CS drugs, they may be given on alternating days to limit disruption of the HPA axis while still producing their therapeutic effect. This limits the possibility of iatrogenic adrenal insufficiency

36
Q

Describe metabolic adverse effects of prolonged corticosteroid administration

A
  • Through various effects may cause hyperglycemia (steroid diabetes)
  • causes peripheral muscle wasting and increased central fat deposition; face, back of neck, supraclavicular region, leading to a cushingoid appearance.
37
Q

Describe electrolyte and water disturbances associated with long term corticosteroid administration

A
  • Increased sodium and water retention which may lead to hypertension
  • increased potassium excretion
  • increased calcium excretion which may lead to osteoporosis
38
Q

Describe adverse effects of CS administration on the CNS, GI, and respiratory systems

A
  • CNS: may cause behavioural disturbances, euphoria, psychosis
  • GI effects: peptic ulcers
  • Respiratoy: decreased surfactant production in neonates
39
Q

Deltasone (Prednisone)

A
  • Intermediate acting corticosteroid
  • Causes broad anti-inflammatory effects
    • Decreases eicosanoid production
    • Decreases inflammatory cytokine production
    • Decreases inflammatory cell produciton and recruitment
    • Reduces histamine production and release
  • Used to treat cancer, inflammation, allergy, and autoimmune disorders
  • Prolonged use may disrupt HPA axis and lead to addisonian crisis when withdrawn
40
Q

Cortef / Solu-Cortef (Hydrocortisone)

A
  • Short-acting corticosteroid
  • Causes broad anti-inflammatory effects
    • Decreases eicosanoid production
    • Decreases inflammatory cytokine production
    • Decreases inflammatory cell produciton and recruitment
    • Reduces histamine production and release
  • Short-acting CS mainly used in CS-replacement therapy (addison’s) or as topical anti-inflammatory
  • Prolonged use may disrupt HPA axis and lead to addisonian crisis when withdrawn
41
Q

Decadron (Dexamethasone)

A
  • Long-acting, high-potency corticosteroid
  • Causes broad anti-inflammatory effects
    • Decreases eicosanoid production
    • Decreases inflammatory cytokine production
    • Decreases inflammatory cell produciton and recruitment
    • Reduces histamine production and release
  • Used in dexamethasone suppression test and in long-term anti-inflammation, anti-immune treatment
  • Prolonged use may disrupt HPA axis and lead to addisonian crisis when withdrawn
42
Q

Describe the three common biologic pathways involved in the development of PAH

A
  • Nitric Oxide: NO-producing enzymes (eNOS) is decreased in PAH patients
  • Prostaglandin: Decreased presence of PGI2 (prostacyclin) producing enzyme
  • Endothelin: Increased ET1 (endothelin) production

All of these pathways lead to smooth muscle contraction and vasoconstriction in the pulmonary arteries. This may lead to thromboembolism in situ

43
Q

The 5 common treatment modalities of PAH are:

A
  • CCBs
  • Prostacyclin
  • Endothelin receptor antagonists
  • Nitric oxide donors
  • PDE-5 inhibitors (sildenafil)
44
Q

The preferred route of drug administration when treating PAH is:

A

inhalational

45
Q

Describe the use of iNO in PAH management

A
  • Given as an inhaled gas (iNO = inhaled NO)
  • Any NO that diffused into blood is bound to Hb and deactivated (little to no systemic effects)
  • NO causes pulmonary arterial vasodilation and inhibits platelet aggregation
46
Q

The chemical mediators that are most associated with production of pain, inflammation, and fever are:

A

The prostaglandins (PG)

HLTH 2511 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions