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Bio58 Final > Questions 17-40 p1 > Flashcards

Questions 17-40 p1 Flashcards

1
Q

What are sedatives?

A

A drug that reduces the desire for physical activity

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2
Q

What are hypnotics?

A

A drug that induces and maintains sleep/unconsciousness

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3
Q

How many cycles of sleep are there?

A

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

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4
Q

How long is a full sleep cycle?

A

60-90 minutes

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5
Q

How many stages in NREM?

A

4

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6
Q

Tell me all about Stage 1 in NREM sleep

A

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

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7
Q

Tell me all about Stage 2 in NREM sleep

A

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

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8
Q

Tell me all about Stages 3 & 4 in NREM sleep

A

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

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9
Q

Tell me all about REM?

A

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

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10
Q

What is the MOA of Benzodiazepines?

A

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

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11
Q

How do BZD’s affect the sleep cycle?

A

Increase Stage 2
Decrease Stage 4
NO effect on REM

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12
Q

What is the MOA for barbiturates?

A
  1. inhibit the reticular formation

2. inhibit activity in the cerebral cortex

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13
Q

How do barbiturates affect the sleep cycle?

A

Increase Stage 2
Decreases Stages 3 & 4
Suppresses REM

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14
Q

How many stages of anesthesia are there?

A

4

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15
Q

What happens in anesthesia in Stage 1?

A

Depression of Cerebral Cortex = euphoria

Unconsciousness

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16
Q

What happens in anesthesia in Stage 2?

A

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

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17
Q

What happens in anesthesia in Stage 3?

A

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

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18
Q

What happens in anesthesia in Stage 4?

A

“Medullary Paralysis”

Complete CNS depression/Coma/Death

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19
Q

Describe the steps of the inflammatory process?

A

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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20
Q

What is prostaglandin responsible for?

A
  1. MAIN inflammation mediator

2. Pain - signals from PNS to CNS

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21
Q

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

A
  1. synthesized on demand in small qty (NOT Stored)
  2. short half-life (rapid degradation0
  3. local effects only (NOT circulated)
  4. inhibition of PG reduces pain and inflammation
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22
Q

What does COX stand for and what is it?

A

Cyclo-oxygenase

An enzyme that SYNTHESIZES prostaglandin

23
Q

How many COX receptors are there and where are they?

A

Cox 1 - mainly stomach

Cox 2 - mainly everywhere else

24
Q

What is GOUT?

A

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

25
Q

At what joints do you typically find GOUT?

A
  1. Big Toe

2. Kidney Joint

26
Q

How does the body actually make GOUT worse?

A

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
27
Q

Name the 4 drug categories to treat GOUT.

A
  1. Anti-Gout
  2. Hypouricemic
  3. Anti-Inflammatory
  4. Uricosuric
28
Q

Name the drug and MOA for Anti-Gout category

A

Colchichine

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

29
Q

Name the drug and MOA for Hypouricemics

A

Allopurine, Febuxostat

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

30
Q

Name the drug and MOA for anti-inflammatory

A

Indomethacin

MOA = NSAID (cox 1 and 2 inhibitor)

31
Q

Name the drug and MOA for uricosuric

A

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

32
Q

What are TCA’s and their MOA?

A

Tricyclic Antidepressants

MOA = inhibit reuptake of NE and Serotonin

33
Q

What are MAOI’s and their MOA?

A

Monoamine oxidase inhibitors

MOA = inhibit degradation of Dopamine, NE & EPI

34
Q

What are SSRI’s and their MOA?

A

Selective Serotonin Reuptake Inhibitors

MOA = inhibit reuptake of selective serotonin

35
Q

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

A

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)

36
Q

What is the etiology of depression?

A
  1. Major Catastrophic Life Event
  2. Genetics
  3. Enivornmental
37
Q

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

A
  1. depressed mood most of the day

2. Anhedonia (markedly diminished interest in normal daily liked activities)

38
Q

How is Major Depressive Disorder diagnosed?

A

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
39
Q

How is depression treated?

A

with medications to balance the following neurotransmitters:

  1. Dopamine
  2. NE
    e. Serotonin
40
Q

What is psychosis?

A

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

41
Q

Which neurotransmitter is responsible for psychosis?

A

Excessive Dopamine transmission

42
Q

Which receptors do antiemetics block?

A
  1. D2 receptors in the CTZ

2. Histamine Receptors

43
Q

What is the MOA for cardiac glycosides?

A
  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
44
Q

What condition are cardiac glycosides used for?

A

CHF

45
Q

What is THE cardiac glycoside to know?

A

Degoxsin

46
Q

What does decreasing the preload mean?

A

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

47
Q

What does decreasing the afterload mean?

A

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

48
Q

What is renin?

A

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

49
Q

What substance does Renin directly stimulate the formation of?

A

Angiotensin I

Previously in the blood as angiotensinogen

50
Q

What is the MOA of Loop Diuretics?

A

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

51
Q

List 3 important things regarding Loop Diuretic profiles

A
  1. aka Organic Acid Diuretics
  2. more potent than thiazide
  3. usually NOT Mixed with other diuretics
  4. can cause hypokalemia
52
Q

What is especially monitored when people are taking loop diuretics?

A

Blood for hypokalemia

53
Q

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

A
  1. Renal Disease
  2. Edema
  3. CHF

Bio58 Final (9 decks)

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