Questions 17-40 p1 Flashcards by amy valine

What are sedatives?

A drug that reduces the desire for physical activity

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What are hypnotics?

A drug that induces and maintains sleep/unconsciousness

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How many cycles of sleep are there?

2 cycles
NREM (Non-rapid Eye Movement)
REM (Rapid Eye Movement)

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How long is a full sleep cycle?

60-90 minutes

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How many stages in NREM?

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Tell me all about Stage 1 in NREM sleep

5% of total cycle
Awake, settling
Muscle activity low
light sleep

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Tell me all about Stage 2 in NREM sleep

50% of total cycle
Asleep, but easily awakened
Respiratory and HR slow

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Tell me all about Stages 3 & 4 in NREM sleep

“Physical Rest and Restoration”
20% of total cycle
Delta Brain Waves
Deep & Very Deep Sleep

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Tell me all about REM?

“Mental Rest and Restoration”
25% of total cycle (approx. 20 min)
Brain speeds up = dreaming

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What is the MOA of Benzodiazepines?

create sedation by enhancing the inhibitory effects of GAMA (gamma aminobutyric acid)

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How do BZD’s affect the sleep cycle?

Increase Stage 2
Decrease Stage 4
NO effect on REM

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What is the MOA for barbiturates?

inhibit the reticular formation

2. inhibit activity in the cerebral cortex

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How do barbiturates affect the sleep cycle?

Increase Stage 2
Decreases Stages 3 & 4
Suppresses REM

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How many stages of anesthesia are there?

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What happens in anesthesia in Stage 1?

Depression of Cerebral Cortex = euphoria

Unconsciousness

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What happens in anesthesia in Stage 2?

“Excitement Phase”
complete depression of Cerebral Cortex
Hypothalamus takes over, HR & BP increase

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What happens in anesthesia in Stage 3?

“Best Stage for Surgery”
Hypothalamus depressed as well
HR & BP return to normal, relatively still depressed

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What happens in anesthesia in Stage 4?

“Medullary Paralysis”

Complete CNS depression/Coma/Death

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Describe the steps of the inflammatory process?

Injury to body/tissues releases the following:
1. Histamine (released from masts & basophils)
2. Bradykinin (inflammation mediator/pain signal)
3. Prostaglandin
THIS all sends pain signals to CNS and through vasodilation phagocytes come to are to clean

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What is prostaglandin responsible for?

MAIN inflammation mediator

2. Pain - signals from PNS to CNS

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What are the 4 things to know about PG’s?

synthesized on demand in small qty (NOT Stored)
short half-life (rapid degradation0
local effects only (NOT circulated)
inhibition of PG reduces pain and inflammation

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What does COX stand for and what is it?

Cyclo-oxygenase

An enzyme that SYNTHESIZES prostaglandin

How many COX receptors are there and where are they?

Cox 1 - mainly stomach

Cox 2 - mainly everywhere else

What is GOUT?

A metabolic disorder characterized by high levels of uric acid in the blood from metabolism of nucleic acids in proteins.

At what joints do you typically find GOUT?

1. Big Toe | 2. Kidney Joint

How does the body actually make GOUT worse?

By trying to rid the body of foreign antigens, phagocytes come to the area BUT make it more acidic which: 1. makes crystals grow bigger (like loves like) 2. pain 3. inflammation

Name the 4 drug categories to treat GOUT.

1. Anti-Gout 2. Hypouricemic 3. Anti-Inflammatory 4. Uricosuric

Name the drug and MOA for Anti-Gout category

Colchichine | MOA = inhibits phagocytes from coming to area and making situation worse

Name the drug and MOA for Hypouricemics

Allopurine, Febuxostat | MOA = inhibits xanthinine oxidase from breaking down hydroxanthinine into uric acid and excretes it in feces

Name the drug and MOA for anti-inflammatory

Indomethacin | MOA = NSAID (cox 1 and 2 inhibitor)

Name the drug and MOA for uricosuric

Probenecid MOA = 1. enhances excretion of uric acid 2. inhibits re-absorption of uric acid

What are TCA's and their MOA?

Tricyclic Antidepressants | MOA = inhibit reuptake of NE and Serotonin

What are MAOI's and their MOA?

Monoamine oxidase inhibitors | MOA = inhibit degradation of Dopamine, NE & EPI

What are SSRI's and their MOA?

Selective Serotonin Reuptake Inhibitors | MOA = inhibit reuptake of selective serotonin

What are the NEW GENERATION anti-depressants and their MOA?

Trazodone & Nefazodone (inhibits reuptake of NE & Serotonin) Venlafaxine (inhibits reuptake of Dop, NE & Ser) Bupropion (inhibit reuptake of dopamine) Mirtazapine (RELEASES more NE and Ser)

What is the etiology of depression?

1. Major Catastrophic Life Event 2. Genetics 3. Enivornmental

What are the 2 general symptoms you MUST have 1 of?

1. depressed mood most of the day | 2. Anhedonia (markedly diminished interest in normal daily liked activities)

How is Major Depressive Disorder diagnosed?

Must have 1 of the 2 PLUS 4 of the 7 for more than 2 weeks! 1. 5% weight gain/loss 2. sleep issue (insomnia/hypersomnia) 3. fatigue/lethargy 4. psychomotor stimulation 5. feelings of worthlessness or guilt 6. difficulty concentrating/thinking 7. repeated thoughts of death/suicide/attempts

How is depression treated?

with medications to balance the following neurotransmitters: 1. Dopamine 2. NE e. Serotonin

What is psychosis?

An impaired mental function which INTERFERES with normal daily activities characterized by bizzare behavior and a deterioration in personality.

Which neurotransmitter is responsible for psychosis?

Excessive Dopamine transmission

Which receptors do antiemetics block?

1. D2 receptors in the CTZ | 2. Histamine Receptors

What is the MOA for cardiac glycosides?

1. inhibits ATPase, which inhibits Na+ from leaving cell WHICH 2. enhances entrance of Ca++ WHICH 3. increases force of contraction WITHOUT consuming more oxygen

What condition are cardiac glycosides used for?

CHF

What is THE cardiac glycoside to know?

Degoxsin

What does decreasing the preload mean?

Dilating the veins so there is not so much return to the right chamber and less pre-fill of the ventricles

What does decreasing the afterload mean?

Dilating the arteries so there is less peripheral resistance and its easier to eject blood, leaving less in the ventricles

What is renin?

An enzyme produced by the kidney when bp or Na+ levels are low at the juxtoglomerular apparatus.

What substance does Renin directly stimulate the formation of?

Angiotensin I | Previously in the blood as angiotensinogen

What is the MOA of Loop Diuretics?

Work on the asencding limb of the loop of henle to inhibit re-absorption of Na+ and Cl-, hence less water re-absorpted THEREBY lowering volume and pressure of blood plasma

List 3 important things regarding Loop Diuretic profiles

1. aka Organic Acid Diuretics 2. more potent than thiazide 3. usually NOT Mixed with other diuretics 4. can cause hypokalemia

What is especially monitored when people are taking loop diuretics?

Blood for hypokalemia

What are the CLINICAL INDICATIONS that call for the use of loop diuretics?

1. Renal Disease 2. Edema 3. CHF