Test three Flashcards

1
Q

What do ACE inhibitors do?

A

relax veins and arteries to lower blood pressure
they do this by stopping angiotensin II production
Also prevent or reverse pathological changes in heart and blood vessels

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2
Q

common side effect vs adverse effects of ace inhibitors

A

cough bc increased bradykinin

first dose hypotension
teratogenic
angioedema –> fucks up airway

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3
Q

ARBs

A

less effective than ACEis, but work similarly
also block aldosterone
no cough

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4
Q

ARB side effects

A

Low bp
Other (fatigue, dizzy, headache)
Swelling
Allergic rxn
Raised K
Teratogenic
AKI (drops perfusion)
Nasal congestion

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5
Q

Who should you NOT give CCBs to?

A

HF patients

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6
Q

Where do CCBs work?
-which conditions are they good for?

A

heart and blood vessels (not so much veins)
reduce work
good for angina and afib

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7
Q

How do CCBs work?

A

decrease AV conduction
slow HR and force of contraction
reduce afterload
increase coronary perfusion

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8
Q

examples of CCBs

A

verapamil and diltiazem

Nifedipine is a hard core one

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9
Q

How to identify CCB OD

A

dizzy, headache, nausea, face flushing

EKG

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10
Q

How do vasodilators reduce cardiac workload?

A

act on arteries to reduce afterload

act on veins to reduce preload

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11
Q

Adverse side effect of vasodilators

A

reflex tachycardia –> increases O2 demand

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12
Q

examples of vasodilators

A

hydrazaline

Sodium nitroprusside
-fast acting drip for emergencies
-can cause cyanide poisoning

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13
Q

Treatment choices in order for htn

A

lifestyle mod, diuretic, vasodilator, ACEi, BB, CCB

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14
Q

Why shouldn’t you use salt substitutes if htn?

A

they usually contain K which activates the RAAS

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15
Q

Which drug classes are prohibited in pregnant ppl with htn?

A

ACEi, ARBs, DRIs

(use BBs instead)

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16
Q

Nitrates use for angina

A

dilate everything
don’t mix with ED meds
tablets dissolve (no first pass effect)
take off at night

17
Q

stable vs unstable angina

A

stable= predictable (e.g. after exercise)
unstable = random –> happens at rest

18
Q

Anti-ischemia therapy

A

MONA (morphine, O2, Nitroglycerine, aspirin)

also BBs and ACEis

19
Q

if a patient is on aspirin and they come in with GI bleed and their platelet is normal, do they need more platelets?

A

yes –> js bc platelets are there doesn’t mean they’re working

aspirin deactivates them

20
Q

side effects of BBs (why aren’t ppl complient?)

A

ED, weird dreams, depression, fatigue

21
Q

anticoagulants vs antiplatelets vs thrombolytics

A
  1. disrupt coagulation cascade, suppressing fibrin (heparin)
  2. inhibit platelet aggregation (aspirin)
  3. promote lysis of fibrin
22
Q

heparin vs LMWH

A

both are made from animals and act on platelets and thrombin

LMWH works slower –> once dailly –> longer half life
heparin works super fast –> small half life

both bad for renal patients bc kidney excretion

23
Q

Warfarin

A

anticoagulant
Super variable –> gotta get labs done all the time
Vit K antagonist
Takes forever to kick in, so you gotta start with enoxaparin

24
Q

Antidotes for heparin and warfarin

A

heparin: protamine sulfate (also platelet infusion)

warfarin: Vit K or fresh frozen plasma

25
Q

goal INR for anticoagulant therapy?

A

2-3

26
Q

Direct thrombin inhibitors
-example

A

Dabigatran and bivalirudin

take once a day and its not affected by lifestyle
No antidote though

27
Q

What do tPAs do and when should you use them?

A

break down clots
only use in emergencies (MI, stroke, massive PE)

28
Q

What’s the only type of isotonic soln

A

plasmalight

29
Q

Lets talk ab K and how it gets fucked up

A

K gets fucked up if you pee too much (kidneys regulate it)
insulin helps remedy hyperkalemia (give sugar with it)
K a/w acidosis
give 10 meq/100cc/hr

30
Q

Lets talk ab Mg and how it gets fucked up

A

diarrhea and alcoholism cause low Mg
kidney pts and L&D usually have high Mg
Mg relaxes muscles (that’s why it’s used in preeclampsia)

31
Q

2 major things that htn causes

A

HF and afib

32
Q

diuretics help w/ preload or afterload?
how about RAAS inhibitors?

A

preload
afterload

33
Q

Digoxin and Cardiac glycosides

A

-inotropes
-digoxin has super narrow therapeutic range and long half life (1.5 days)
adverse effects are dysrhythmias