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Flashcards in Pharmacology Deck (48):
1

autonomic pharmacology schema

Nervous system:
2 branches = somatic (voluntary function, skeletal m.) and autonomic (involuntary, BP, digestion, thermoregulation);

Autonomic NS:
2 branches = sympathetic (mobilizes body energy) and parasympathetic (conserves/stores body energy)

2

autonomic reflexes

allows autonomic integration and control over various physiological functions;

including GI function, BP, and thermoregulation;

dependent upon sympathetic and parasympathetic adjustments

3

baroreceptor reflex

important for controlling BP;

baroreceptors (pressure sensors) located in larger arteries of thorax and neck monitor BP and HR changes;

If a BP drop is sensed, info is relayed to brainstem, which signals an increase in sympathetic discharge to heart and peripheral vasculature AND parasympathetic outflow to heart is decreased

BP = CO x PVR
CO = HR x SV

4

adrenergic receptors at norepinephrine synapses schema

NE --> adrenergic receptor:
2 branches = alpha and beta

alpha = alpha-1 and alpha-2

beta = beta-1, beta-2, and beta-3

5

alpha-1 - primary locations and responses (6)

- intestinal smooth muscle = relaxation,
- vascular smooth muscle = contraction,
- radial muscle iris = contraction,
- urinary sphincter = contraction,
- spleen capsule = contraction,
- ureters = increased motility

6

alpha-2 - primary locations and responses (5)

- CNS inhibitory synapses = decreased sympathetic discharge from CNS,
- pre-synaptic terminal at peripheral adrenergic synapses = decreased NE release,
- GI tract = decreased motility and secretion,
- pancreatic islet cells = decreased insulin secretion,
- some arteries (skeletal m., liver, kidneys) = vasoconstriction

7

beta-1 - primary locations and responses (3)

- cardiac m. = increased HR and contractility,
- kidney = increased renin secretion,
- fat cells = increased lipolysis

8

beta-2 - primary locations and responses (6)

- bronchiole smooth m. = relaxation/bronchodilation,
- some arterioles (skeletal m., liver) = vasodilation,
- GI smooth m. = decreased motility,
- skeletal m. and liver cells = increased cellular metabolism,
- uterus - relaxation,
- gallbladder - relaxation

9

beta-3 - primary locations and responses (3)

- fat cells = increased lipolysis,
- bladder = decreased contraction of detrusor m.,
- heart = decreased contractility

10

hypertension

sustained, reproducible increase in BP;

occurs in 30% of US pop, >20 y/o;

left untreated, leads to CV problems, renal disease, and blindness;

normal BP maintained by: BP = CO x TPR

11

pre-hypertension numbers

120-139 SBP/ 80-89 DBP

12

hypertension numbers

stage 1 =
140-159 SBP/ 90-99 DBP

stage 2 =
>/= 160 SBP/ >/= 100 DBP

13

pathogenesis of primary hypertension

AKA essential HTN = unknown cause, but most likely due to combo of factors;

factors = diet, stress, smoking, alcohol abuse, metabolic syndrome, genetic predisposition;

sympathetic NS = final common denominator; initially increases CO, later increase PVR;

increased BP overtime causes adaptive changes in vessels;

changes = wall thickening, increased reaction to pressor substances, defect in production of vasoactive substances by cells lining peripheral vasculature;

vasodilators = nitric oxide, bradykinin, prostaglandin I1

vasconstrictors = angiotensin II and endothelin-I

14

pathogenesis of secondary hypertension

secondary = unknown cause (chronic kidney disease)

15

diuretics

work on kidney to increase excretion of sodium and water;

16

3 types of diuretics

three types = thiazide, loop, and potassium sparing

17

diuretic ADRs (6+)

- fluid depletion,
- electrolyte imbalance,
- impaired glucose and lipid metabolism,
- GI disturbances,
- weakness/fatigue,
- orthostatic HTN

(spironolactone may cause gynecomastia and hyperkalemia)

18

thiazide diuretics

work in distal tubule to block sodium reabsorption;

osmotic forces cause the nephron to retain more water;

both sodium and water are excreted from the body (?);

examples: hydrochlorothiazide (HCTZ) and metolazone

19

loop diuretics

work in loop of Henle blocking sodium and chloride reabsorption;

examples: furosemide and torsemide

20

potassium-sparing diuretics

interfere with exchange of sodium and potassium in the distal tubule;

sodium is then excreted and potassium loss is reduced;

examples: spironolactone and triamterene

21

beta blockers

reduce workload on the heart, used after MI to help heart recover

beta-1 receptors increase heart rate and cardiac contractility when stimulated;

blocking these receptors decrease HR and contractility;

end in -lol

22

beta-1 selective meds (4)

Atenolol, Bisoprolol, Metoprolol, Nebivolol

23

Non-selective beta blocker meds

has equal affinity for beta-1 and beta-2 receptors;

Carvedilol, Propanolol

24

beta blocker ADRs (6)

- bronchioconstriction
- excessive depression of HR and cardiac contractility
- orthostatic hypotension
- depression
- fatigue
- GI disturbances

25

alpha blockers

alpha-1 adrenergic receptors stimulation causes vascular smooth muscle contraction;

blocking these receptors decreases vascular resistance;

also used to treat benign prostatic hypertrophy (BPH) b/c it decreases contraction of smooth muscle in prostate allowing men to void more easily

26

Alfuzosin and Tamsolosin

alpha blockers;

selective for alpha receptors on smooth muscle in prostate and lower urinary tract

27

Doxazosin

alpha blocker;

highly alpha-1 selective;

promotes relaxation of smooth muscle in vasculature, decreasing PVR

28

Prazosin

alpha blocker;

used for hypertension

29

alpha blocker ADRs (3)

- reflex tachycardia
- orthostatic hypertension
- increased risk of cardiac disease

30

centrally acting agents (Clonidine)

inhibit sympathetic discharge from the brainstem;

stimulation of alpha-2 receptors cause decrease in sympathetic discharge to heart and vasculature

31

centrally acting agents (Clonidine) ADRs (3)

- dry mouth
- dizziness
- sedation

32

vasodilators

inhibit smooth muscle contraction by increasing intracellular production of cGMP and other messengers;

increased cGMP inhibits contraction of smooth m. leading to vasodilation;

vasodilation decreases BP by decrease PVR

33

vasodilator meds (3)

Hydralazine and Minoxidil for resistant HTN;

Nitroprusside for pts in hypertensive crisis

34

vasodilator ADRs (7+)

- reflex tachycardia
- dizziness
- orthostatic hypotension
- weakness
- nausea
- fluid retention
- headache
*Minoxidil also causes hair growth; AKA Rogaine

35

renin-angiotensin system inhibitors

includes:
- ACE inhibitors
- angiotensin II receptor blockers
- direct renin inhibitor

system = angiotensinogen --> (renin) --> angiotensin I --> (ACE) --> angiotensis II

36

angiotensin II causes:

- vasoconstriction (increase BP)
- increase aldosterone (increase salt and H2O retention)
- vascular remodeling and hypertrophy (thickened vascular wall leading to additional resistance to blood flow that causes increase HTN)

37

ACE inhibitors

prevent conversion of angiotensin I to angiotensin II;

end in -pril

38

ACE inhibitor meds (10)

- Enlapril
- Ramirpril
- Lisinopril
- Benazepril
- Moexipril
- Captopril
- Perindopril
- Quinapril
- Fosinopril
- Trandolapril

39

angiotensin II receptor blockers

block angiotensin II from binding to receptors;

end in -sartan

40

angiotensin II receptor blocker meds (7)

- Losartan
- Valsartan
- Irbesartan
- Telmisartan
- Candesartan
- Azilsartan
- Olmesartan

41

direct renin inhibitor

prevents renin from converting agiotensinogen to angiotensin I

42

direct renin inhibitor med (1)

aliskiren (Tekturna)

43

renin-angiotensin system inhibitors ADRs

- dry cough (not ARBs)
- hematological effects (neutropenia, agranulocytosis)
- renal problems (glomerulonephritis, renal failure)
- angioedema (welts, burning/itching, facial swelling, dyspnea)

44

calcium channel blockers
(two types)

- dihydropyridine agents
- non-dihydropyridine

45

dihydropyridine
(calcium channel blocker)

block calcium entry into vascular smooth muscle;

inhibits contraction that leads to vasodilation;

ends in -pine

46

dihydropyridine meds (3)

- Amlodipine
- Nifedipine
- Felodipine

47

non-dihydropyridine
(calcium channel blocker)

has greater effect on calcium influx into myocardial cells;

primary effect = decreased HR and myocardial contraction

48

calcium channel blockers ADRs

- excessive vasodilation (swelling)
- orthostatic hypotension
- abnormal heart rate
- reflex tachycardia
- dizziness
- headache