ILE I Exam I HTN Flashcards
Miscellaneous facts I'm afraid of forgetting lol
1
Q
SOAP
A
- Subjective 2. Objective 3. Assessment 4. Plan
2
Q
ADE
A
Can be allergies, ADRs, medication errors, overdoses
3
Q
ADRs
A
Any injury or unpleasant side effect resulting from APPROPRIATE use of a medication
4
Q
Hypotension
A
<90/<60
5
Q
5 Steps for NT
A
- Biosynthesis
- Storage
- Release
- Receptor interaction
- Termination
6
Q
Sympathetic NT
A
NE (some ACh)
7
Q
Parasympathetic NT
A
ACh
8
Q
Sympathetic effect on eyes
A
mydriasis
9
Q
parasympathetic effect on eyes
A
mitosis
10
Q
sympathetic effect on saliva
A
decreased production
11
Q
sympathetic effect on SV and HR
A
increased
12
Q
Parasympathetic effect on vasculature
A
None! :p
13
Q
Sympathetic effect on vasculature
A
vasoconstrict
14
Q
Sympathetic effect on liver
A
glycogen -> glucose
15
Q
Parasympathetic effect on liver
A
bile production
16
Q
Receptor found in lungs
A
B2
17
Q
Receptor found in heart
A
B1
18
Q
Parasympathetic nerve form
A
Long, short
19
Q
Sympathetic nerve form
A
Short, long
20
Q
mecamylamine and trimethaphan work at what point on the nerve?
A
Presynaptic
21
Q
sweat glands have what innervation?
A
sympathetic (ACh -> M)
22
Q
Blood vessels, cardiac tissue, SA/AV nodes, exocrine glands and eye muscles have what innervation?
A
Sympathetic (NE -> a, b)
23
Q
SA/AV nodes, GI smooth muscle, bronchioles, eye muscles have what innervation?
A
parasympathetic (ACh -> M)
24
Q
Tubocurare and succinylcholine work at what point in the nerve?
A
NMJ
25
Adrenergic receptor types
A1 (A1A, A1B, A1C), A2 (A2A, A2B, A2C), B (B1, B2, B3)
26
Which cells release renin?
JG cells (juxtaglomerular) (in kidney)
27
Which cells "wake up" JG cells?
Macula densa cells
28
With what do macula densa cells wake up JG cells?
prostaglandins (act locally)
29
What produces angiotensinogen
Liver cells
30
Angiotensinogen + renin
AT1
31
6 types of drug interactions
1. Ion-ion
2. Ion-Dipole
3. Dipole-dipole
4. Hydrophobic
5. Pi
6. pi-cation
32
Which receptor interactions are the strongest?
ionic
33
Intrahepatic recycling
Drugs that are excreted from bile and reabsorbed by the portal vein
34
Which electrolytes are lost when taking first-line anti-hypertensives?
Na, K, Mg, Cl,
35
The excretion of which 2 substances decrease when taking first-line anti-hypertensives
Ca, Uric acid
36
Which drugs mentioned in class are thiazides?
HCTZ, chlorthalidone
37
how do thiazides work?
Sulfonamide (-SO2NH) donates proton and has a negative charge, which competes with Cl-
38
DHP drug(s) mentioned in class
Amlodipine
39
Non-DHP drug(s) mentioned in class
Verapamil and diltiazem
40
DHP or non-DHP affects the heart as well as vasculature
Non-DHP
41
What is the reflex response experienced by patients taking CCB?
When taking DHP, carotid artery sense BP drop. NE released
42
Reflex response is experienced when taking DHP or non-DHP?
DHP only
43
How do CCBs work?
Block Ca2+ flow into vascular muscle/SA node, decreasing heart rate
44
Adverse effects of CCBs
Hypotension, Constipation, Muscle weakness, Flushing, Swelling in the lower extremities, Gingival hyperplasia, Headache
45
Bradykinin is produced when
ACE inhibitors block AT1->AT2
46
which anti-hypertensive causes cough? why?
ACEI, ARBs,
| bradykinin buildup
47
Which 2 ACEI were mentioned in class?
Enalapril, captopril
48
ACEI MOA
Block AT1 -> AT2, block bradykinin breakdown
49
One of the 2 ACEI mentioned in class is a prodrug. Which one?
Enalapril (esters -> COOH)
50
Taste disturbance is caused by which drug class?
ACEI
51
Swelling of lower extremities is caused by which drug class?
CCB
52
What does AT2 do?
Produces aldosterone and causes vasoconstriction
53
Why would you use an ARB over an ACEI?
ARBs cause less coughing (but still a problem)
54
Does bradykinin breakdown occur when taking an ACEI? An ARB?
ACEI - no
| ARB - yes!
55
Angioedema occurs much less with (ACEI/ARB) than with (ACEI/ARB)
much less with ARBs
56
Which drugs mentioned in class are ARBs?
-Valsartan (any -sartan)
57
ARB MOA
ATII antagonist at ATI receptor
58
Adverse effects of ARBs
Hypotension, Dizziness, Headache, Nausea and Vomiting (N/V), Cough, Increased K+ levels, Decreased GFR.
59
OBRA purpose
Requires drug utilization reviews to lessen medication costs and errors
60
OBRA introduced 3 requirements for pharmacists. What were they?
1. Prospective DUR review
2. Patient counseling
3. Record keeping
61
Beta blockers side effects
Bradycardia, Sedation, Fatigue, Shortness of Breath (SOB), Headache, Sleep Disturbances, Sexual Dysfunction
62
BB MOA
Blocks B1 receptor in heart -> Decreased heart rate, Decreased central sympathetic outflow, Decreased Renin release
63
Direct vasodilators MOA
open potassium channels resulting in hyperpolarization of vascular smooth muscle. Inside of cell becomes more negative as K leaves
64
Side effects of direct vasodilators
hypotension, reflex response, hypertrichosis (minoxidil)
65
Direct vasodilators presented in class
Minoxidil, hydralazine
66
SA node is controlled by ___ which is controlled by ___ which has ___ receptors
SA node is controlled by vagal nerve, which is controlled by the vasomotor center, which has A2 receptors
67
Centrally acting antihypertensives (CAA) MOA
Decrease sympathetic outflow, many are A2 antagonists
68
CAAs adverse effects
Sedation, Bradycardia, Constipation, Dry mouth, Dizziness
69
Decreased venous return does what to BP? Do CAAs cause a decrease in venous return?
decreased venous return = lower BP, yes
70
CAAs mentioned in class
Clonidine, alpha-methyl-dopa, alpha-methyl-norepinephrine
71
Loop diuretic MOA
The loop diuretics are the most powerful diuretics known due primarily to their site of action. Inhibition of the Na+/1K+/2Cl- symport results in a powerful diuretic effect resulting in the loss of these ions along with Ca+2 and Mg+2.
72
Most powerful diuretic
Loop diuretic
73
Adverse effects of loop diuretics
electrolyte imbalance
74
Loop diuretics mentioned in class
Lasix
75
Loop diuretics vs thiazide diuretics; which causes loss of Ca?
Loop
76
Aldosterone antagonist MOA
inhibit aldosterone mediated stimulation of ENaC and Na+/ATPase synthesis resulting in increased Na+ excretion and decreased K+ excretion.
77
A1 antagonists
inhibit A1 receptors in vasculature, allowing them to vasodilator
78
A1 antagonists
Terazosin
