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Integrated Medical Sciences > Pharmacology > Flashcards

Pharmacology Flashcards

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USMLE® Step 1 flashcards
1
Q

Agonist of muscarinic receptor

A

Muscarine

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2
Q

Antagonist of muscarinic receptor

A

Atropine

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3
Q

Agonist of nicotinic receptor

A

Nicotine

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4
Q

Antagonist of nicotinic receptor

A

Curare

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5
Q

Is a muscarininc receptor a G protein coupled or NT gated receptor?

A

G-protein coupled

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6
Q

Is a nicotinic receptor a G protein coupled or NT gated receptor?

A

NT gated

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7
Q

Is an adrenergic receptor a G protein coupled or NT gated receptor?

A

G-protein coupled

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8
Q

What is ACh made from? What enzyme?

A 
Choline and Acetyl CoA
Choline acetyltransferase (ChAT)
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9
Q

What is ACh broken down into? What enzyme?

A

Choline and Acetic Acid

Acetylcholinesterase (AChE)

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10
Q

Sympathetic NS is which spinal levels?

A

T1-L2

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11
Q

Parasympathetic NS is which spinal levels?

A

Brain stem, S2-S4

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12
Q

What are the subtypes of nicotinic receptors?

A

Neuronal, muscle

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13
Q

What are the subtypes of muscarinic receptors?

A 
M1 (gastric parietal cells)
M2 (heart - negative chronotropic effects)
M3 (GIT, lacrimal)
M4 (adrenal medulla, CNS)
M5 (CNS)
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14
Q

What does vesamicol?
What NT does it affect?
Does it increase or decrease activity?

A

Prevent ACh packing into vesicles?
ACh
Decrease

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15
Q

What does botulinum toxin do?
What NT does it affect?
Does it increase or decrease activity?

A

Prevents attachment/exocytosis of vesicles from presynaptic neuron?
ACh
Decrease

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16
Q

What does hemicholinium do?
What NT does it affect?
Does it increase or decrease activity?

A

Prevents re-uptake of choline to pre-synaptic neuron
ACh
Decrease

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17
Q

Tubocurarine

A

Compete with ACh for nicotinic ACh receptor
ACh
Decrease

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18
Q

Atropine

A

Compete with ACh for muscarinic ACh receptor
ACh
Decrease

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19
Q

Anticholinesterases

A

Inhibit breakdown of ACh to choline and acetic acid
ACh
INCREASE

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20
Q

What are the effects of NE binding to alpha 1 receptors?

A

EXCITATORY

Vasoconstriction (except heart, skeletal muscle, liver)
Sphincters close
Arrestor pilli contract
Radial muscle of pupil dilates

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21
Q

What are the effects of NE binding to alpha 2 receptors?

A

INHIBITORY

Feedback inhibition = inhibit NE release
Increase glucagon –> increase glucose

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22
Q

What are the effects of NE binding to beta 1 receptors?

A

HEART
Increase HR, increase contractility –> increase CO

KIDNEY
Increase renin –> increase BP

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23
Q

What are the effects of NE binding to beta 2 receptors?

A

Smooth muscle relaxation
LUNGS - bronchodilation
HEART, SKELETAL MUSCLE, LIVER - dilation

Increase glycogenolysis and gluconeogenesis –> increase glucose

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24
Q

What are the effects of NE binding to beta 3 receptors?

A

Lipolysis at adipose tissue

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25
Q

In blood vessels:

Alpha 1 receptors are found ____________ and are stimulated by _____________.
Beta 2 receptors are found ____________ and are stimulated by _____________.

A

Alpha 1 receptors are found NEAR THE NERVE and are stimulated by NERVES

Beta 2 receptors are found THROUGHOUT THE VESSEL and are stimulated by ADRENALINE FROM THE ADRENAL MEDULLA

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26
Q

At low epinephrine levels…..

At high epinephrine levels….

A

At low epinephrine levels - B2 are occupied (have high affinity –> dilation)

At high epinephrine levels - A1 are occupied (more of them –> constriction)

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27
Q

What do MAO inhibitors do?
What NT does it affect?
Does it increase or decrease activity?

A

Antidepressants
Prevent action of monoamine oxidase (MAO) in pre-synaptic neuron (i.e., prevents NE breakdown)
NE
Increase

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28
Q

What do COMT inhibitors do?
What NT does it affect?
Does it increase or decrease activity?

A

Anti-parkinson’s
Prevent action of COMT in post-synaptic neuron (i.e., prevents NE breakdown)
NE
Increase

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29
Q

What do NE re-uptake inhibitors do? EXAMPLE?
What NT does it affect?
Does it increase or decrease activity?

A

E.g., coccaine
Prevent re-uptake of NE to pre-synaptic neuron
NE
Increase

30
Q

What does reserpine do?
What NT does it affect?
Does it increase or decrease activity?

A

Prevents packaging of NE into vesicles?
NE
Decrease

31
Q

What does alpha-meethyltryosine do?
What NT does it affect?
Does it increase or decrease activity?

A

Mimics and competes with tyrosine (precursor for NE - i.e., disrupts NE synthesis)
NE
Decrease

32
Q

What drugs end in “—pril”?

A

ACE inhibitors

33
Q

What drugs end in “—sartan”?

A

Angiotensin receptor antagonist / blocker (ARBs)

34
Q

What drugs end in “—iren”?

A

Renin inhibitors

35
Q

What drugs end in “—ones”?

A

Potassium sparing diuretics

36
Q

What drugs end in “—olol” or “—alol”?

A

B adrenergic receptor blockers

i.e., beta blockers

37
Q

What is the apoprotein on LDL?

What about the receptor to which it binds?

A

ApoB-100

ApoB-100 receptor

38
Q

What is uptake by HDL?

A

Non-esterified cholesterol

39
Q

What is the LDL subtype that underpins atherogenesis?

A

Lp(a)

40
Q

What does Lp(a) do?

A

It resembles and competes with plasminogen.

Plasminogen can be activated to plasmin which dissolves clots.

Lp(a) instead reduces plasmin –> promoting thrombosis

41
Q

What effect do statins have on dyslipiademia?

A

Decrease LDL, TG

Increase HDL

42
Q

What is contraindicated with statins?

A

P450 is an enzyme involved in statin metabolism

Drugs/grapefruit inhibiting P450 microsomal enzymes MUST be avoided (otherwise statin levels increase)

43
Q

What effect do statins have on liver enzymes?

A

Increase

44
Q

Use of statins and fibrates increase the risk of….

A

Myositis (inflammation of skeletal muscle)

Rhabdomyolysis (potentially fatal skeletal muscle breakdown, and renal toxicity, due to myoglobin)

45
Q

What effect do fibrates have on dyslipiademia?

A

Large decrease in TG
Modest decrease in LDL
Modest increase in HDL

46
Q

How do fibrates work?

A

Bind and activates nuclear receptor (PPARa) which:

  • increases synthesis of lipoprotein lipase
  • increase LDL uptake by liver
  • decrease VLDL production by liver
47
Q

How do statins work?

A

Inhibit cholesterol synthesis in liver (ENDOGENOUS) - competitive inhibition of HMG-CoA reductase

Decreased cholesterol –> increased expression of LDL receptors in liver –> clearance of LDL from blood

48
Q

Can bile acid binding resins be taken orally? How do they work?

A

YES - but they are not absorbed
Interfere with administration of fat soluble vitamins and some drugs (anion exchange resin, resin bound bile acids are excreted - not absorbed, liver obligated to form new bile acids from cholesterol –> decreasing serum LDL)

Also reduces cholesterol absorption from intestine

49
Q

What % of bile acids are usually reabsorbed?

A

90-95%

50
Q

Can ezetimibie be taken orally? How do they work?

A

YES - it is absorbed
DOES NOT interfere with absorption of fat soluble vitamins
Adjunct treatment to statins (endogenous) whereas ezetimibie is (exogenous)

Inhibits sterol carrier protein required for cholesterol absorption –> decreased absorption of cholesterol –> decreased LDL in liver –> increases LDL clearance from plasma to liver

51
Q

What do omega 3 fish oils do?

A

Decrease TG
Decrease clotting
Decrease inflammation

Requires high dose

52
Q

What does nicotinic acid do?

A

Decrease LDL
Increase HDL

BUT requires very high dose - not well tolerated

53
Q

What % of O2 consumption does heart use?

What % of cardiac output does heart receive?

A

11%

4% - relatively poorly perfused

54
Q

Name three vasodilators?

Name one vasoconstrictor?

A

NO
PGI2
PGE2 (dilators)

Endothelia 1 (constrict)

55
Q

Do nitrates dilate arteries or veins more?

A

Veins

56
Q

Can nitrates be taken orally?

A

NO - significant hepatic first pass metabolism - degraded

They are taken via sublingual administration or transdermal patches

57
Q

How long do short acting vs long acting nitrates last?

A

30 mins

4-6 hrs

58
Q

What drug can be used as prophylactic treatment of angina?

A

B antagonists (beta blockers)

59
Q

AMI treatment is aimed at ________, via:

A

repercussion

clot busters (fibrinolytic therapy)
angioplasty (stent)
60
Q

How is an AMI diagnosed?

A

Typical rise and fall of biochemical marker (troponin, CKMB)

AND one of the following:

  • ischaemic symptoms
  • ECG changes
  • coronary artery intervention
61
Q

Times for CK…

A

Increase in 3-6 hrs

Peaks 16-30 hrs

62
Q

True or false?

CKMB mass index is better than CKMB activity?

A

True

BUT - concurrent skeletal muscle injury masks rise in CKMB due to AMI
Unreliable if Total CK

63
Q

Times for aspartate aminotransferase…

A

Appears 6-8 hrs
Peak 24-48 hrs
Return to baseline 4-6 days

64
Q

Times for myoglobin…

A 
Early appearance (2-3 hrs)
Peak 6-9 hrs
Rapid clearance - return to baseline (36 hrs)
65
Q

Times for troponin…

A

Early rise 3-6 hrs

Long diastolic window (7-10 days) - due to bimodal release

66
Q

What does it mean if CK doesn’t go up, but troponin does?

A

Likely to be unstable angina - due to the fact that troponin is very sensitive and can detect minimal injury

67
Q

BNP assay has an excellent ____________

A

negative predictive value (rules out HF as a cause of dyspnea)

68
Q

What does the LAD artery supply?

A

Apex, anterior LV, IV septum

69
Q

What does the LCX artery supply?

A

LV lateral wall

70
Q

What does the RCA supply?

A

RV, posterior LV, IV septum

Integrated Medical Sciences (1 decks)

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