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AAW - CRAAB 1 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

5 specific examples of circulatory shock

A

Cardiogenic shock
Cardiac pumping compromised -> decreased CO
Ex: severe arrhythmias, abrupt valve malfunction, MI, coronary occlusions

Hypovolemic shock
Depletion of body fluids -> decreased blood volume -> reduced cardiac filling -> reduced SV
Ex: significant hemorrhage (>20% blood volume), fluid loss from severe burns, chronic diarrhea, prolonged vomiting

Anaphylactic shock
Severe allergic reaction to antigen sensitivity -> release of histamine, prostaglandins, leukotrienes, bradykinin -> increased arteriolar vasodilation -> increased microvascular permeability -> loss of venous tone -> decreased TPR and CO

Septic shock
Severe vasodilation due to release of substances into blood stream by infective agents.
Ex: endotoxin released from bacteria induces formation of a nitric oxide synthase in endothelial cells

Neurogenic shock
Loss of vascular tone due to inhibition of normal tonic activity of sympathetic vasoconstrictor nerves
Ex: deep general anesthesia, reflex response to deep pain associated with traumatic injury
May also be accompanied by increased vagal activity -> decreased HR; this shock is called “vasovagal syncope”

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2
Q

define autotransfusion

A

a reduced capillary hydrostatic pressure resulting from intense arteriolar constriction

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3
Q

why do people breath rapid and shallowly when they are in circulatory shock

A

because they are using the respiratory pump in order to get blood through the lungs more quickely

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4
Q

how does the liver help out when the body is in circulatory shock?

A

increases glycogenolysis in order to increase blood osmolarity

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5
Q

what are your EFs like in systolic heart failure

A

lower duh

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6
Q

What is the term for autoimmune pericarditis that results a significant time after an MI (on the order of weeks to months)

A

dressler’s pericarditis

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7
Q

how big does the LV wall have to get in order for it to be considered hypertrophic

A

> 1.5 cm

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8
Q

what happens after left ventricle hypertrophy that can lead fo further failure

A

LV dilatation

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9
Q

causes of isolated right sided hypertensive heart disease (cor pulmonale)

how big does the RV have to be in order for it to be hypertrophied

A

Due to chronically ↑ pulmonary artery pressure from:

  • ***chronic pulmonary parenchymal disease: COPD, interstitial fibrosing diseases (sarcoidosis)
  • chronic hypoxia with or without lung disease (e.g. sleep apnea) (causing pulmonary vasoconstriction)
  • pulmonary vascular disease: primary pulmonary hypertension and chronic recurrent thromboemboli

(RV free wall > 0.5 cm)

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10
Q

R-sided IE usually caused by

A

I.V. drug abuse

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11
Q

connective tissue diseases that can cause valve deformations

A

Reumatoid arthritis, ankylosing spondylitis,

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12
Q

atrioventricular valve insufficiency can be due to what give 2 examples

A
  • CHF (causing valve ring dilatation)
  • papillary muscle dysfunction (from LV ischemia due to
    coronary disease)
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13
Q

most common primary cardiac neoplasia

A

atrial myxoma (usually left atrium)

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14
Q

tuberous sclerosis

A

bunch of tumors everywhere that are benign. caused by mutation in tumor supressor proteins. causes rhabdomyomas (benign tumor in striated muscle like cardiac muscle) in children - most common form of primary cardiac cancer in children

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15
Q

where do most metastisies to the heart go?

A

in the pericardium

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16
Q

where do catacholamines come from aka pathway from AA to epi

A

Phenylalanine —phenylalanine hydroxylase—>
tyrasine —tyrosine hydroxylase—>
dihydroxyphenylalanine (DOPA) —-DOPA decarboxylase—>
dopamine —vitamin c & dopamine beta hydroxylase—>
NE —SAM—> Epi

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17
Q

what does the preganglionic adernergic nerve relsease

A

ACh

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18
Q

what is the difference between somatic nerves coming off of the spinal cord and adrenergic nerves coming off the spinal cord

A

Adrenergic - has preganglionic nerves coming off the spinal cord and ganglia in the periphery. sympathetic ganglion have nicotinic receptors that ACh binds to.

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19
Q

what happens to the postganglionic nerve when ACh hits it?

A

sodium comes in, causes action potential propagation via calcium ion gated channels. Vesicles dock with the membrane at the end of the neuron and NE spills out.

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20
Q

when would you want to measure vanillylmandelic acid in the urine

A

pheochromocytoma, catacholamine secreting tumor

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21
Q

isoproterinol

A

activates beta 1 and 2 adrenergic receptors

increases heart rate and lowers resistance (can lower BP because of beta 2 action)

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22
Q

phenylephrine

A

alpha 1 agonist
only one used clinically

used as a vasoconstrictor and nasal decongestant

increases BP

If given with an alpha blocker, it does nothing

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23
Q

alpha 1 antagonists

A

things that end in azosin

terazosin
prazosin
doxazosin

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24
Q

Dobutamine

A

Selective B1 agonist
positive inotrope
increases contractility, increases SV and BP

if you wanted to boost the SV in a heart failure patient you could give this in the hospital

increases BP

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25
Q

B2 activators

used for what
which ones delay labor

A

Albuterol, Metaproterenol, Salmeterol, Ritodrine, Terbutaline,

brochodilation for asthma (except ritodrine)

lowers blood pressure, causes tachycardia, tremors

Ritodrine and terbutaline delay labor.

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26
Q

propanolol

A

non selective beta 1 and 2 antagonist

blocks the B2 activators like albuterol

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27
Q

mech of furosemide

A

NKCC pump inhibitor

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28
Q

“3 drugs that help with heart failure”

according to trachte

A 
ACE inhibitor (lisinopril, etc)
Beta blocker (metoprolol, etc)
Aldosterone receptor inhibitor (spironolactone)
29
Q

What happens if you are an an alpha 1 antagonist and you give epi?

A

Their blood pressure TANKS YA DINGUS

epi acts on alpha 1 and 2, and beta 1 and 2. if you aren’t constricting the vessels with alpha 1, it will act on the others to collectively lower you BP

30
Q

a few common Selective beta 1 blockers

A

metoprolol, atenolol

31
Q

Why use beta 1 selective over non selective beta blockers

A

blocking beta-2 can cause bronchoconstriction and peripheral vasoconstriction

32
Q

Do you ever give a aspecific aterial dilator in heart failure? Why

A

(Like hydralazine) No.

You need a venoilator in order to decrease the preload on the heart

33
Q

Isosorbide mononitrate vs nitro. Whats the difference

A

iso half life is 5hr

nitro is 3 min

34
Q

What is something other than rheumatic fever that can cause mitral valve disorders that we talked about in class

A

enterovirus. Can occur with pregnancy

35
Q

Pargyline

A

MAOI, inhibits monoamine oxidase, causing NE to stay in the cleft longer. blocks type b MAO

36
Q

Reserpine

A

inhibits the granular pump that accumulates catacholamines in vesicles, resulting in a depletion of catecholamines

(used to be used to treat PB but has severe psychological SE)

37
Q

cocaine effects on CNS

A

inhibits the axoplasmic pump (which usually uptakes the NE)

38
Q

phenelzine

A

MAOI, causing NE to stay in the cleft longer

39
Q

Guanethidine

A

goes into the nerve ending via the axoplasmic pump, once inside, it depletes the NE stores, reducing response to sympathetic stimulation.

*inactive in the presence of inhibitors of the the axoplasmic pump

40
Q

People on ____ should not eat cheese beer and wine, because they contain ____

A

people on MAOIs should not eat beer cheese and wine because they contain Tyramine, which releases catacholamines (via reversal of axoplasmic transporter) that cannot be degraded by MAO (because it is inhibited).

41
Q

two different types of monoamine oxidases

A

A - in intestine and brain, blocked by perlindole

B - in various organs, blocked by seligeline and pargyline

42
Q

function of alpha 1 receptors and the degree to which they are sensitive to different catacholimes

A

epinephrine > norepinephrine&raquo_space; isoproterenol
mediates smooth muscle contraction (primary Cardiovascular location is blood vessels)
activates phospholipase C (Gaq dependent process)
To increase intracellular calcium via inositol trisphosphate

43
Q

function of alpha 2 receptors and the degree to which they are sensitive to different catacholimes

A

epinephrine > norepinephrine&raquo_space; isoproterenol
inhibition of neural norepinephrine release
prejunctional nerve terminal, platelets, gut, medulla oblongata
acts to decrease cAMP or activate Na/H antiporter
G protein alphai dependent process

44
Q

function of beta 1 receptors and the degree to which they are sensitive to different catacholimes

A

isoproterenol > epinephrine = norepinephrine
adrenergic cardiac effects (increase in rate and contractility), renin release
located in heart, JG apparatus & adipose tissue
acts to increase cAMP via G protein alpha subunit

45
Q

function of beta 2 receptors and the degree to which they are sensitive to different catacholimes

A

isoproterenol > epinephrine&raquo_space; norepinephrine
relaxation of smooth muscle & metabolic (glycogenolytic) effects
primary site in cardiovascular system is blood vessels (smooth muscle in general)
LUNGS
acts to increase cAMP via G protein alpha subunit

46
Q

Intropin (trachte calls it inotropin)

A

dopamine HCL

At low [], beta 1 agonist (positive inotropic effect)
at high [], alpha 1 agonist

use for shock to maintain renal perfusion, also can be used for hypotension

47
Q

what does agonizing a dopaminergic receptor do

A

dilation of renal and mesenteric vasculature

48
Q

drug name for NE

A

levophed bitartrate

49
Q

if you gave NE after an alpha 1 blocker, what would happen to BP

A

it would still go up, just not as much. The NE effects on B1 are MUCH stronger than their effects on B2, so the increase in HR would outweigh the decrease in TPR.

50
Q

Ephedrine

A

noncatecholamine sympathomimetic general agonist

releases norepi

used to treat bronchospasm, vasoconstricts and reduces mucosal congestion via alpha 1

51
Q

Pseudoephedrine

A

sterioisomer of ephedrine used to treat nasal decongestion

52
Q

things that reverse the axoplasmic transporter

A

Tyramine, amphetamine, ephedrine

53
Q

imipramine

A

TCA!

Block the axoplasmic pump

54
Q

normal PR, QRS, and QT intervals

A

o PRI - P-R Interval(where P wave starts and Where QRS Complex starts) .12-.20 sec

o QRS –

55
Q

Supraventricular tachycardia

A

QRS

56
Q

PACs

A

premature atrial contraction

you can still see the p wave

57
Q

first degree block

A

PR > .2sec

58
Q

second degree block type one

A

PR gets longer and longer UNTIL there is a dropped QRS complex, as in it didn’t show up!

59
Q

second degree block type two

A

same as type one, but the pr interval is fixed the whole time. (it doesn’t get longer and longer)

60
Q

junctional escape rhythm

A

atria arent contracting, ventricles take over at like 40-60

sometimes no p wave

61
Q

Accelerated junctional rhythm

A

same as jucntional rhythm, but 60-100bpm

inverted p waves

62
Q

Ventricular escape beat/ ventricular bradycardia

A

enlarged QRS

ventricles are controlling the rhythm

63
Q

agonal rhythm

A
64
Q

PVC

A

premature ventricular contraction

early ventricular beat, it has a widened QRS

65
Q

ACE inhibitors

A

lisinopril

Enalapril

66
Q

Hydralazine

A

increaswes NO synthesis in endothelium, higher selevtivity for arterioles = decreased afterload

67
Q

example of an aldosterone receptor antagonist

A

Spironolactone

68
Q

Digoxin

A

Inhibits Na/K ATPase:
• Increased Na intracellular concentration
• Increased Na/Ca co-transporter activity
• Increased intracellular Ca++
• INCREASED CONTRACTILIY (positive ionotrope)
ALSO – prolongs nodal action potentials thus DECREASING HEART RATE

VERY HIGH TOXICITY

AAW - CRAAB 1 (8 decks)

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