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Pharm Final Review > Overall Review > Flashcards

Overall Review Flashcards

1
Q

Intranasal (localized or systemic)

A 
localized drug action
CNS effect (preparation dependent)
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2
Q

inhalation

A

can be systemic or localized

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3
Q

facilitated diffusion and Active transport

A

hydrophilic, large, ionized

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4
Q

factors affecting absorption

A
  1. molecular characteristics (charge, size, lipophilicity vs hydrophilicity)
  2. administration route
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5
Q

Absorption and Distribution

A

lipophilic, small, and non-ionized

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6
Q

Excretion

A

hydrophilic, ionized

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7
Q

First Pass

A

PO –> hepatic vein –> systemic body

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8
Q

Examples of first pass metabolism

A

morphine, meperidine, diazepam, midazolam, lidocaine, propranolol, ETOH

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9
Q

Factors affecting distribution

A
  1. PPB
  2. size of tissue
  3. blood flow to the tissue
  4. molecular characteristics
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10
Q

Albumin

A

acidic drug

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11
Q

Alpha 1 acid glycoprotein

A

basic drug

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12
Q

Highly bounded PPB Examples

A

Warfarin, NSAID, ibuprofen, naproxen, furosemide, digitoxin

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13
Q

Blood brain barrier

A

selective transport

P-glycoprotein pump

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14
Q

volume of distribution (Vd)

A

drug dose/ measured drug plasma concentration

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15
Q

inactive drug to active metabolite

A

prodrug

ig. codeine

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16
Q

active drug to active metabolite

A

toxic

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17
Q

Phases of metabolism

A

phase I: hydrolysis, reduction, oxidation (Cytochrome P450 group)

polar metabolite: ionized, saturable

Phase II: conjugation, polarization

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18
Q

Inhibitors of CYP 450 1A2

A

Ciprofloxacin (inhibit metabolism)

-decrease metabolism -> manage diarrhea symptoms

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19
Q

Inducers of CYP 450 1A2

A

Barbituates
Cruciferous vegetables
Tobacco
(increased metabolism)

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20
Q

example of phase ii metabolism (induce metabolism)

A

acetaminophen (tylenol) is phase I metabolized to N-acetyl-p-benzoquinoneimine (which is hepatotoxic), and then phase II is metabolized by glutathione enzyme conjugation to an inactive metabolite.

p.s. overdose can lead to depletion of glutathione –> TOXIC

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21
Q

what are the excretory organs?

A

kidney (primary), saliva, bile, lungs.

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22
Q

3 factors affecting renal excretion

A
  1. molecular characteristics (PPB, Urinary pH, metabolized)
  2. renal function (young vs old)
  3. cardiac output (renal blood flow)
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23
Q

first order kinetics

A

readily metabolized in the liver

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24
Q

zero order kinetics

A

metabolism is saturable
e.g. ETOH, aspirin, phenytoin

1-2 drinks = 20-30 mg/dL
clearance rate = 20mg/dL/hr
ETOH poisoning: > 295mg/dL

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25
Q

creatinine

A

checks your kidney function by looking at the amount of creatinine in your urine and blood.

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26
Q

half-life

A

time at which drug has lost half its Cmax concentration

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27
Q

examples of narrow TI meds

A

warfarin
dignoxin
phenytoin
tacrolimus

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28
Q

partial agonist

A

lower efficacy

eg. buprenorphine (less effect than opioid)

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29
Q

inverse agonist

A

bind to the agonist site but produce the opposite effect

eg. caffine (inhibit the effect of adenosine, which prompts GABA release to inhibit wakefulness)

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30
Q

antagonist

A

blocks the receptor site but NO efficacy

e.g. naloxone (for opioid misuse)

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31
Q

Common overdose drugs examples

A 
acetylsalicylic acid (aspirin)
acetaminophen (tylenol)
fentanyl
cocaine
benzodiazepines
alcohol
antidepressants
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32
Q

overdose procedure

A 
airway
breathing
circulation (perfusion)
disability (dysfunction)
exposure
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33
Q

toxidromes

A

toxic syndromes and signs

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34
Q

acetylsalicylic acid

A

function: decrease platelet aggregation （一直失血)

confusion
tachycardia
tachypnea
hyperthermia
diaphoresis 發汗
vomiting
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35
Q

acetaminophen

A 
abdominal pain
loss of appetite
nausea/vomiting
diaphoresis
somnolence 嗜睡
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36
Q

opioids

A 
bradypnea/apnea
bradycardia
somnolence/coma
pupils constricted
itching (allergic response relating to inflammation)
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37
Q

cocaine (stimulant)

A 
agitation, tremors
tachycardia
tachypnea
hyperthermia
diaphoresis
pupil dilated

tx: sedatives

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38
Q

adsorption

A

activated charcoal
binding of drug to decrease its absorption

e.g. tylenol poisoning, asa, benzodiazepines

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39
Q

ways to increase elimination

A
  1. activated charcoal (GI)
  2. urinary alkalization (renal) e.g. acidic aspirin poisoning give sodium bicarbonate
  3. hemodialysis (renal)
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40
Q

Parietal cells and gastric chief cells synthesize and secrete

A

HCL acid / Pepsinogen –> pepsin (active)

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41
Q

How do endogenous organs be protected from gastric juice

A

foveolar cells have mucous and bicarbonate, bile and pancreatic bicarbonate

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42
Q

What’s the pH of GI? and pH after HCO3?

A

1.5-3.5, to 7

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43
Q

HCI positive feedback

A

Enteroendorine (G) cells –> gastrin
gastrin stimulates parietal cells
parietal cells produce HCI
HCI is released by proton pump into stomach
proton pump is mediated by enzyme H+K+-ATPase

G cells release histamine
histamine binds to H2 receptors on parietal cells
parietal cells increase HCI production

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44
Q

GERD pathophysiology (2)

A
  1. weak lower esophageal sphincter
  2. delayed gastric emptying

–> mucosal injury

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45
Q

GERD treatment (3)

A
  1. decrease acidity
  2. avoid irritants
  3. fundoplication (tight pylorus)
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46
Q

PUD pathophysiology

A

failure of endogenous protection (cell junctions and mucous/bicarbonate layer)

–> mucosal erosion

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47
Q

Treatment for H pylori

A

amoxicillin

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48
Q

Where does H pylori present in?

A

present in both 90% duodenal and 75% gastric ulcers

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49
Q

ranitidine
cimetidine
famotidine

A

H2 receptor antagonists

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50
Q

antibiotics to treat PUD

A

amoxicillin
clarithromycin
metronidazole

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51
Q

pepto bismol 3 utilization

A

antiinfective
antiacid
antidiarrheal

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52
Q

large intestine synthesizes what vitamins

A

vitamin b and k

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53
Q

noninflammatory vs inflammatory acute diarrhea

A

< 2 weeks

inflammatory is caused by pathogenic invasion of intestinal cells, infectious, have fever and bloody diarrhea (dysentery). dehydration

e.g. C. difficile

noninflammatory is disruption of normal absorption, will feel nausea or vomit. dehydration

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54
Q

first and second line c. difficile treatment

A

1st: flagyl (DNA)
2nd: vancomycin(cell wall)

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55
Q

what does atropine mean

A

stimulate sympathetic system and block parasympathetic system –> inhibit GI function

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56
Q

Three types of diarrhea

A
  1. osmotic diarrhea
  2. secretory diarrhea
  3. inflammatory diarrhea
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57
Q

IBS

A

neurologic bowel disorder (diarrhea)
CNS dysregulation of normal motility
triggered by stress, anxiety, etc.

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58
Q

What is Hirschsprung disease

A

ganglion cells in large intestine wall dont develop before birth. –> constipation

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59
Q

Five types of laxatives

A
  1. bulk forming
  2. softeners
  3. saline and osmotic
  4. stimulants
  5. miscellaneous
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60
Q

cathartics

A

evacuation of the bowel for procedure

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61
Q

where is the vomiting centre

A

medulla and outside of BBB

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62
Q

H1 antagonism (antihistamine)

A

reduce vestibular excitation (motion sickness)

dimenhydrinate: diphenhydramine + chlorotheophyline
meclizine (dramamine)
diclectin (pregnancy): doxylamine + pyridoxine hydrochloride (vitamin b6)

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63
Q

antimuscarinic anticholinergics and meds

A

reduce vestibular excitation (motion sickness)

scopolamine - transdermal patch

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64
Q

5HT3 antagonist and meds

A

purpose: visceral pain

ondansetron

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65
Q

D2 receptor antagonism

A

purpose: GI pain

phenothiazines
metoclopramide
prochlorperazine

s/e: sedation

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66
Q

CB1 & 2 agonism

A

purpose: chemotherapy
cannabinoids: THC and cannabidiol

stimulate GABA to inhibit sympathetic activity

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67
Q

Cannabinoids meds

A

Dronabinol
Cesamet
Nabilone
Cannibas

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68
Q

whats the percentage of body fluid

A

60%

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69
Q

percentage of intracellular fluid

A

40%

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70
Q

percentage of extracellular fluid

A

20%

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71
Q

What to do when GI bleeding

A

stop contributing meds like antiplatelet, anticoagulants, thrombolytics, NSAIDs

give fluids and blood transfusion

give proton pump inhibitor

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72
Q

Expected osmolality

A

275 to 295 mOsm/kgH20

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73
Q

Osmolality is dependent on

A

number of dissolved solutes

dehydration= higher = more solutes
over-hydration = lesser = less solutes
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74
Q

Tonicity focuses on

A

sodium and dextrose amount in IV fluid

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75
Q

albumin 5% fluid tonicity

A

isotonic in the bag and hypertonic in the body

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76
Q

D5 1/2 NS fluid tonicity

A

hypertonic in the bag and isotonic in the body (dextrose is quickly utilized

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77
Q

how much fluid is needed for maintenance?

A

35ml/kg/day of water (grown adult)

4/2/1 rule

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78
Q

how much glucose is needed to limit starvation ketosis

A

50-100g/day

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79
Q

NPO meaning

A

nothing by mouth

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80
Q

colloids

A

aka. plasma expanders
supply protein into ECF and stays in circulation
e.g. plasbumin, alburex

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81
Q

treatment for hypovolemic shock

A

colloids

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82
Q

NS 0.9% contents and side effects

A

154 mEq Na
154 mEq CI
isotonic

hypokalemia and no dextrose (lack energy)

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83
Q

what is #1 choice for resuscitation fluid?

A

NS 0.9% adults 500mL

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84
Q

Lactated Ringer content

A

more electrolytes

potassium 4mEq
Calcium 2.7 mEq
lactate 28mEq

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85
Q

LR is not suitable for which population? why?

A

children; too high electrolytes, high lactate

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86
Q

D5NS and D5LR tonicity

A

hypertonic

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87
Q

Dextran 40 tonicity

A

isotonic, but hypertonic in the body

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88
Q

D10W tonicity

A

hypertonic

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89
Q

D5 0.45% NS

A

hypertonic; osmolality = 405 mOsm/L

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90
Q

25% albumin tonicity and treatment

A

hypertonic; resuscitation to replace deficits (IV volume expander)

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91
Q

3% NaCl tonicity and treatment

A

hypertonic; head injury to lower ICP

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92
Q

what is the first choice for maintenance fluid for pediatrics

A

D5 0.45% NS (requires electrolytes and dextrose)

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93
Q

0.45% NS tonicity

A

hypotonic

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94
Q

D5W tonicity

A

hypotonic in body but isotonic in bag

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95
Q

3.3% dextrose, 0.3% sodium

A

hypotonic

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96
Q

D5 0.2% NS

A

hypotonic

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97
Q

Electrolytes balance is important for?

A

nerve conduction and water balance

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98
Q

common causes and treatment of
Hyponatremia
Hypernatremia

A

<135 mEq/L; diuretics; D5NS

145 mEq/L; kidney failure; diuretics

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99
Q

common causes and treatment of
Hypokalemia
Hyperkalemia

A

< 3.5 mEq/L; diuretics; KCL IV/PO

>5 mEq/L; K+ sparing diuretics; Kayexalate

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100
Q

tx of diabetic ketoacidosis

A

hypotonic fluid

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101
Q

tx of hypernatremia

A

hypotonic fluid

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102
Q

tx of cerebral edema

A

hypertonic fluid

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103
Q

tx of severe hyponatremia

A

hypertonic fluid

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104
Q

tx for dehydration patients d/t vomiting and diarrhea

A

isotonic LR

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105
Q

preeclampsia

A

gestational HTN

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106
Q

causes of gestational HTN

A

inflammatory cytokine release due to endothelial changes

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107
Q

risk of gestational HTN

A

DIC, thrombocytopenia

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108
Q

decreased elasticity of vessels = _____ peripheral vascular resistance

A

increased

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109
Q

orthostatic hypotension

A

drop of SBP <20mmHg or DBP >10mmHg
120/80 normal –> 100/70

venous pooling, transient

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110
Q

treatment of orthostatic hypotension

A

adrenergic agonists

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111
Q

Mean arterial pressure

A

70-100mmHg

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112
Q

CO=

A

CO=SV x HR

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113
Q

CPP=

A

MAP - ICP
map: usually the same
ICP: increase

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114
Q

whats the treatment of HTN (ER)

A

nitric oxide (direct acting vasodilator)

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115
Q

Meds for nitric oxide; s/e

A

nipride and hydralazine

syncope (fainting), hypotension due to reflex tachycardia

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116
Q

4 types of treatment for HTN

A

diuretics
renin angiotensin drugs (ACE inhibitors and angiotensin II receptor blockers) (vasodilate and decrease blood volulme)
calcium channel blockers (decrease CO)
adrengeric agents (decrease CO and vasoconstriction)

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117
Q

whats is 1st line HTN treatment

A

diuretics

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118
Q

4 types of diuretics

A
  1. Loop diuretics (furosemide) ascending loop of henle
  2. Thiazides distal convoluted tubule
  3. Potassium sparing (spironolactone) collecting duct –> increases na out and keep k+ in
  4. Osmotic (mannitol, isosorbide) proximal tubule and loop of henle–> pull solvent into circulation and into renal tubules & inhibit renin release
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119
Q

Aldactazide is a combination of ___ and ___ and excellent ______ therapy for HTN

A

thiazide and k+ sparing combination; maintenance

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120
Q

side effects of diuretics and loop specifically

A

hyperglycemia; ototoxicity

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121
Q

in vasoconstriction, liver produces _____ in _____ and kidney produces ______ in response to low BP.

A

angiotensionogen in plasma

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122
Q

how does angiotensinogen converts to angiotensin I

A

by renin

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123
Q

what does adrenal cortex produce?

A

aldosterone (increase sodium reabsorption)

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124
Q

what lead to the production of aldosterone?

A

angiotensin II in plasma

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125
Q

decrease ventricular

A

decrease BP

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126
Q

decrease preload

A

decrease blood volume

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127
Q

angiotensin II binds to receptors

A

blood vessels and heart, adrenal cortex, kidneys

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128
Q

1st line drug in heart failure

A

angiotensin converting enzyme inhibitors –> vasodilate

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129
Q

meds: thiazide diuretic + angiotensin receptor blocker

A

Hyazaar HCT; Cosart-H

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130
Q

treatment of angina and arrhythmias

A

calcium channel blockers

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131
Q

two types of calcium channel blockers

A
  1. vascular selective (smooth)

2. cardio selective (cardiac)

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132
Q

treatment of arrhythmia and atrial fibrillation

A

cardio selective calcium channel blockers and beta blockers

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133
Q

Verapamil and diltiazem

A

cardiac muscle

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134
Q

Nifedipine and amlodipine

A

smooth muscle

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135
Q

adverse effects of calcium channel blockers

A

reflex tachycardia, peripheral edema, dysrhythmias, heart failure, hypotension

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136
Q

ginseng

A

calcium channel antagonist

= ca2+ influx blocked

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137
Q

alpha 1 receptors function

A

cause vasoconstriction

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138
Q

alpha 2 receptors function

A

cause vasoconstriction

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139
Q

beta 1 receptors function

A

increase cardiac activity (HR)

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140
Q

beta 2 receptors function

A

bronchodilation and vasodilation

increased breakdown of glycogen to supply energy

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141
Q

specificity:
atenolol
propranolol
metoprolol

A

beta 1 vosodilation

beta 1 and beta 2 antiarrhythmic (

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142
Q

what is the adrenergic antagonist meds for antiarrhythmic

A

propranolol

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143
Q

specificity:
Prazosin
Phentolamine

A

(alpha 1) – peripheral vasodilation

(alpha) – peripheral vasodilation

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144
Q

lopressor HCT

A

diuretic (thiazide) and adrenergic antagonist

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145
Q

how does CNS alpha 2 adrenergic agonists work? what does it inhibit?

A

decreased in sympathetic tone by decreasing presynaptic ca levels –> inhibiting release of norepinephrine

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146
Q

whats the treatment for resistant HTN

A

CNS alpha 2 adrenergic agonist

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147
Q

what lead to endothelial cell damage (clotting)

A
  1. mechanical stress
  2. immune response
  3. oxidative stress
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148
Q

Site of injury (high cholesterol level) produce ____

A

VCAM-1

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149
Q

VCAM-1 causes the migration of ____ beneath endothelium

A

circulating monocytes

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150
Q

how is free radical released and what does it impact?

A

monocytes differentiate into macrophages and produce oxidative stress; LDL

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151
Q

oxidized LDL become _____ after phagocytized by ______.

A

form cell; macrophage

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152
Q

what organ and enzyme produces cholesterol?

A

liver; HMG-CoA

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153
Q

drugs lowering lipids (inhibit cholesterol)

A
  1. statins (decrease LDL)
  2. niacin (increase HDL) –> increase clearance
  3. fibrates (decreases VLDL) –> increase lipolysis and metabolism
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154
Q

what is the first line treatment for post MI (myocardial infarction)

A

statin

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155
Q

what lowering lipids med is ideal for low HDL

A

niacins

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156
Q

HMG CoA inhibitor

157
Q

side effects of statin

A

myopathy, CYP2C9 and CYP3A4 enzymes interactions

158
Q

pregnancy category X interferes with

A

fetal CNS myelination

159
Q

oxidative stress is caused by?

A

free radicals (reactive oxygen species)

160
Q

what function does oxidative stress damage? what does it lead to?

A

insulin resistance; inflammation

161
Q

what is formed in antioxidant

A

formation of water molecules

e.g. grape

162
Q

4 types of manifestation of atherosclerosis

A
  1. narrowing of the vessel
  2. vessel obstruction due to plaque
  3. thrombosis
  4. weakening of the vessel wall
163
Q

differences between chronic and acute CAD

A

chronic: stable angina, thick fibrous plaque
acute: unstable angina, risk of MI when plaque rupture due to clotting, unstable plaque

164
Q

4 release signals for aggregation

A
  1. adenosine diphosphate (ADP)
  2. thromboxane A2
  3. Thrombin
  4. Glycoprotein IIB/IIIa receptor activation (make platelet bind)
165
Q

describe coagulation process

A

injured vessel stimulate factor X –> prothrombin activator –>

prothrombin to thrombin

fibrinogen to fibrin

166
Q

thrombin function

A
  1. converts fibrinogen to fibrin
  2. activate factor XIII (13) –> loose to stabilized mesh)
  3. enhances platelet aggregation
  4. facilitates its own synthesis
167
Q

what is essential to blood coagulation

168
Q

clotting treatment

A
  1. antiplatelet
  2. anticoagulant
  3. thrombolytic
169
Q

STEMI

A

ST too high, unable to rest (ventricular fibrillation problem)

170
Q

ischemia

A

decreased blood flow = decreased O2 in the body

171
Q

which intrinsic enzyme appear in plasma first at 3 hrs?

172
Q

injury of myocardial cells can lead to leaking of _______.

A

intrinsic enzymes: troponin, creatine Kinease, myoglobin

173
Q

isosorbide =

A

organic nitrates and osmotics diuretics

174
Q

whats the 1st line acute intervention for angina

A

organic nitrates (3 tablets, 5 min apart)

175
Q

CABG

A

CABG uses blood vessels from another part of the body and connects them to blood vessels above and below the narrowed artery, bypassing the narrowed or blocked coronary arteries.

176
Q

how does antiplatelet work?

A

block thromboxane A2 and block ADP in degranulation

177
Q

meds for antiplatelet

A

ASA
dipyridamole
aggrenox (combination of asa and dipyridamole)
clopidogrel

178
Q

How does ASA work to treat clotting?

A

it blocks COX1 enzyme and therefore inhibit thromboxane production = decreased platelet aggregation

179
Q

How does clopidogrel work to treat clotting?

A

it blocks ADP to decrease platelet adhesion

180
Q

baby aspirin function and recommended doses

A

treat inflammation in blood vessel; 81mg adult and 10-15mg/kg pediatric

181
Q

kawasaki syndrome treatment

A

common in children

baby aspirin

182
Q

how does anticoagulants work?

A

aka. blood thinners;
by inhibiting thrombin (=no fibrin)
blocking thrombin receptors and factors
inhibiting hepatic formation of specific clotting factors (II,VII,IX,X))

183
Q

meds for anticoagulants

A

heparin
low molecular weight heparins (enoxaparin, dalteparin)
dabigatran
warfarin

184
Q

how does heparin work to treat clotting?

A

inhibit thrombin

185
Q

how does dabigatran work to treat clotting?

A

prodrug; block thrombin receptors and factor

186
Q

how does warfarin work to treat clotting

A

inhibit hepatic formation of specific clotting factor (2,7,9,10)

187
Q

how can heparin induced thrombocytopenia occur?

A

immune reaction when heparin antibodies bind to platelet factor 4 to activate platelet and produce a hypercoagulable state
tx: use LMWH

188
Q

what to monitor for warfarin activity

A

prothrombin time

189
Q

what to monitor for heparin activity

A

activated partial thromboplastin time

190
Q

what to monitor for LMWH activity

A

anti factor Xa levels

191
Q

what to monitor for bleeding risk activity

A

complete blood count

192
Q

how does thrombolytics work

A

alteplase
reteplase

tissue plasminogen activator (tPa) allows plasminogen in bloodstream to convert to plasmin = clot (fibrin) lysis

193
Q

5 risk factors of thrombosis

A 
blood stasis (bedrest)
high estrogen (birth control)
smoking
blood clotting disorders (antithrombin III deficiency)
surgery
194
Q

Deep vein thrombosis

A

occurs when a blood clot (thrombus) forms in one or more of the deep veins in your body, usually in your legs.

195
Q

pulmonary embolism is caused by

A

DVT; life threatening

196
Q

treatment of pulmonary embolism

A

prevention is the key (compressino stockings)

ER: thrombolytics

197
Q

what are the 3 cushing triads for ICP?

A

hypertension, bradycardia and apnea

198
Q

cerebral edema can lead to increased ____

199
Q

differences b/w ischemia and hypoxia

A

Ischemia is insufficient blood flow to provide adequate oxygenation.
This leads to tissue hypoxia (reduced oxygen) or anoxia (absence of oxygen).

200
Q

two types of cerebral edema; difference

A

vasogenic: increased permeability (blood brain barrier is disrupted)
cytotoxic: increased ICP

201
Q

which type of cerebral edema is caused by head injury, hematoma, hemorrhage, CNS infection?

202
Q

which type of cerebral edema is caused increased intracellular fluid shift?

203
Q

the most common CVA (stroke)

A

ischemic not hemorrhagic

artery completely blocked

204
Q

transient ischemic attack

A

angina of the brain because artery temporarily blocked

短暫性腦缺血發作

205
Q

what are the treatments for TIA and CVA

A 
thrombolytics within 3 hours since onset
carotid endarterectomy (move plaque from carotid artery)
angioplasty
antiplatelet
anticoagulant
206
Q

the most common artery involved in stroke

A

Middle cerebral artery (limb and face) - part of circle of willis

207
Q

dysarthria

A

weak muscle control

208
Q

apraxia

A

moving the muscles needed in the correct order

209
Q

dyslexia

A

impairment of reading

210
Q

dysgraphia

A

impairment of writing

211
Q

agnosia

A

inability to recognize and identify objects/persons

212
Q

2 risk factors for hemorrhagic CVA

A

atriovenous malformation, aneurysm

213
Q

treatment of hemorrhagic

A

white/red/platelet cell count decreased

stabilize, osmotic diuretics, hypertonic NS, optimize perfusion, surgical evacuation

214
Q

treatment for cerebral edema

A

3% NS & mannitol

215
Q

what is arteriovenous malformation (AVM)?

A

congenital defect in formation of cerebral vessels- lack capillary network

216
Q

problem with AVM?

A

high pressure arterial flow enters venous vessels rapidly –> rupture (hemorrhage)

217
Q

S&S of AVM?

A

steal blood flow from surrounding area –> ischemia –> slow onset neuro deficits

218
Q

treatment of AVM

A

surgical clipping (removal), radiation (Gamma knife), embolization

219
Q

3 locations aneurysm can present in

A

cerebral
aortic abdominal
throacic

220
Q

which part of cerebral does aneurysm largely present in

A

circle of willis (subarachnoid hemorrhage)

221
Q

treatment if aortic aneurysm ruptures

A

systemic bleed: give fluids

222
Q

treatment if cerebral aneurysms ruptures

A

hemorrhagic CVA: surgery

223
Q

treatment of cerebral aneurysm

A

coiling or flow diversion before ruptures (stent directs blood away from the aneurysm itself)

224
Q

what are the interventional meds to prevent thrombus prophylaxis (prevention) post surgery

A
  1. give antiplatelet meds til 3 months post (ASA, clopidogrel)
  2. heparin if high risk for clotting
  3. MRI follow up
  4. smoking cessation
225
Q

what med to give for people with high risk for clotting

226
Q

risk factor for aortic aneurysm in elderly?

A

age: elastin is not synthesized

227
Q

what is cardiac tamponade

A

extra fluid builds up

228
Q

causes of cardiac tamponade

A

aortic aneurysm, cardiac rupture (MI), cardiac intervention, cardiac surgery, trauma

229
Q

what is pericardiocentesis

A

evacuate fluid from heart by needle and catheter to drain

230
Q

what is intracerebral

A

within cerebral lobes

231
Q

causes of hematomas

A

ruptured cerebral aneurysm, AVM, hemorrhagic stroke due to head injury

232
Q

two locations of hematoma?

A

epidural (skull and dural) and subdural (dural and subdural space)

233
Q

what is a common cause of epidural hematoma

A

skull fracture injury

234
Q

what is a common cause of subdural hematoma

A

venous tearing caused by injuries

235
Q

treatment for hematoma

A

decrease ICP, evacuate, 3% NS, mannitol

236
Q

how does cardiac tamponade lead to hypotension then HF?

A

pressure on myocardium –> heart does not stretch out fully between contractions –> chambers dont fill properly –> less CO –> compensatory SNS stimulation –> hypotension and heart failure

237
Q

sign and symptoms of cardiac tamponade

A

pulses paradoxus –> drop in BP with inspiration
WHY?
due to greatly increased left-ventricular afterload

指吸氣時脈搏顯著減弱或消失，系左心室搏血量減少所致(because chambers dont fill properly already)

238
Q

how does starling law apply to pulsus paradoxus?

A

starling law states that the stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction. (and vice versa)

however, in cardiac tamponade, since the heart doesnt stretch out fully due to the buildup of fluids, pulsus paradoxus occur (hypotension with inspiration) as “decreased SV lead to decreased CO” ©=HR x SV)

239
Q

what does adrenal medulla produce

A

catecholamines, adrenaline, noradrenaline

240
Q

what does adrenal cortex produce

A

glucocorticoids (cortisol), aldosterone, androgens

241
Q

s&s of repeated stress?

A

salt craving, hypoglycemia, hyponatremia, fatigue

242
Q

what happen in repeated stress in body?

A

repeat secretion of cortisol –> depletion

243
Q

which organ responds to level of cortisol

A

hypothalamus

244
Q

why is keto diet bad

A

metabolic acidosis:
the liver breaks down fat into ketones –> blood becomes acid

normal blood pH: 7.35 to 7.45

245
Q

chronic risks of ketogenic diet

A

increased LDL cholesterol, kidney stones, decreased growth hormones, renal damage, bone mineral loss

246
Q

differences between primary and secondary pulmonary hypertension

A

primary: idiopathic, hereditary
secdonary: disease

247
Q

heart failure definition

A

condition which decreases the heart’s ability to pump enough blood

248
Q

afterload vs preload

A

preload: the initial stretching of the cardiac myocytes (muscle cells) prior to contraction
afterload: the force or load against which the heart has to contract to eject the blood.

249
Q

what is cor pulmonale

A

(pulmonary artery increases too much)

condition that causes right sided heart failure

250
Q

right heart failure vs left heart failure

A

right (received from venous)
- peripheral, GI, and liver obstruction (aka. congestion)
s/s: anorexia, GI distress, weight loss, impaired liver function, edema

left (received from lung)
- pulmonary obstruction, impaired gas exchange, decreased CO,
s/s: cyanosis, hypoxia, decreased tissue perfusion, cough with sputum

251
Q

what is the most common cause of heart failure?

A

low CO = hypotension

252
Q

How does the body compensate for decreased cardiac output in cases of congestive heart failure?

A

Since SNS activation due to low O2 = worsening of CO…

  1. release endothelial enzymes
    - pulmonary vasoconstriction –> hypertension
    - induce smooth muscle cell and fibroblast proliferation –> hypertrophy = thick and stiff cardiac wall
  2. release inflammatory mediators: cytokines
253
Q

what does compensation of HF lead to?

A

tachycardia and ventricular fibrillation

254
Q

2 pharmacotherapeutics ways to treat HF?

A
  1. decrease cardiac workload and increase O2 supply
    (decrease HR, oxygenate, decrease pre/afterload
  2. increase contractility
255
Q

what are the treatment for HF?

A

decrease HR/BP and increase O2= diuretics, ACE inhibitor, adrenergic antagonists, direct acting, vasodilators, calcium channel antagonists

increase contractility: cardiac glycosides, p inhibitors, adrenergic agonists

256
Q

how does cardiac glycoside work?

A

block exit of Na and increase Ca in cells & slows electric conduction pathway at AV node to decrease HR

result: increased contractility and increased CO

257
Q

how does cardiac glycoside work?

A

block exit of Na and increase Ca in cells & decrease SA-AV node conduction to decrease HR

result: increased contractility and increased CO

258
Q

how do you call the loading dose of digoxin? what to monitor

A

digitalization; narrow TI so monitor HR (apical pulse x 1 minutes)

259
Q

what is the first sign of toxicity for digoxin? whats the antidote?

A

vomiting and nausea; digibind

260
Q

how does Phosphodiesterase inhibitors work?

A

blocks enzyme phosphodiesterase to increase cAMP activity

result: increased contractility in myocardial cells & vasodilation

261
Q

how does Phosphodiesterase inhibitors work?

A

blocks enzyme phosphodiesterase to increase cAMP activity

result: increased contractility in myocardial cells & vasodilation

262
Q

viagra

A

Phosphodiesterase inhibitor to treat erectile dysfunction (increased blood flow)

263
Q

what type of agent is adrenergic agonist

A

sympathomimetic agents

264
Q

how does adrenergic agonists work

A

increase contractility, increase cardiac output, some vasodilation

265
Q

dobutamine action

A

B1 specific: direct sympathomimetic

Dobutamine directly stimulates beta-1 receptors of the heart to increase myocardial contractility and stroke volume, resulting in increased cardiac output.

266
Q

dobutamine action

A

used in acute heart failure

B1 specific: direct sympathomimetic

Dobutamine directly stimulates beta-1 receptors of the heart to increase myocardial contractility and stroke volume, resulting in increased cardiac output.

267
Q

dopamine HCL action

A

used in acute heart failure

non-selective B: precursor to norepinephrine, stimulates catecholemines

dopamine receptor in smooth muscle and in renal beds allow vasodilation

268
Q

3 treatment for acute heart failure; how do they work

A
  1. loop diuretics (furosemide): reduce preload
  2. direct acting vasodilators: increase myocardial oxygenation & decrease preload and afterload
  3. B1 agonists: dobutamine: increase contractility = CO
269
Q

what is dilated cardiomyopathy

A

left ventricle camber is enlarged due to weakened heart muscle

270
Q

risk factor for dilated cardiomyopathy

A

genetics, gender (male 20-50)

271
Q

how to treat dilated cardiomyopathy

A

loop diuretics, direct acting vasodilators, b1 agonists, heart transplant

272
Q

2 treatment for chronic heart failure

A

(longer acting)

  1. cardiac glycosides
  2. ACE/ARBs
273
Q

how does arrhythmias affect cardiac rhythm? (3)

A
  1. re-entry circuits to SA node: Atrial fibrillation; SVT
  2. AV node dysfunction: ventricular fibrillation, QRS blocked
  3. PNS stimulation: vagus nerve leads to bradycardia
274
Q

2 treatment for arrhythmias

A
  1. decrease SA-AV node conduction
    - treatment of atrial fibrillation
    - slow HR
    drugs: digoxin
    intervention: ablation (cut cells that cause arrhythmia)
  2. depress ectopy at ventricular level
    - slows repolarization to enhnace normal AV conduction
    - drugs: lidocaine (Na blocker), amiodarone (k channel blocker)
275
Q

3 treatments of supraventricular tachycardia

A
  1. cardioversion: interruption of ventricular depolarization via low voltage to 調整心律 & use vagal manuvers to stimulate vagus nerve (bradycardia)
  2. adenosine: is a short-acting drug that blocks AV node conduction
  3. antiarrhythmics: decrease HR & slow repolarization
276
Q

what med is used to treat bradycardia

277
Q

what meds are used to treat ventricular fibrillation/tachycardia

A

amiodarone (K channel blocker), lidocaine (Na channel blocker)

278
Q

What type of diabetes is NIDDM

279
Q

DM II

A

increased tissue resistance/insufficient production
pregnancy hormones
pancreatic disease

280
Q

New rise in ____ in DM II

281
Q

how to treat DM II

A

lifestyle, oral antidiabetic agents, insulin

282
Q

If dont treat DM II

A

diabetic ketoacidosis, Hyperosmolar hyperglycemic state (Dehydration)

283
Q

Insulin and glucose treatment for DM II

A

antidiabetic agents

blood glucose: decrease overall blood glucose and increase cellular uptake (Biguanides, SGLT 2 inhibitors)

insulin: increase release and receptor sensitivity

284
Q

why corticosteroids is bad for DM II

A

increase gluconeogenesis and lower insulin receptor affinity

285
Q

Whats the first line therapy for DM II

A

biguanides

286
Q

how does biguanides work

A
  1. increase metabolism to reduce GI glucose absorption

2. alter mitochondrial activity to increase cell glucose uptake and insulin release

287
Q

whats the med for biguanides; onset and peak

A

metformin
onset 2-3 hr
peak 10-16 hr

288
Q

what organs function are important to assess for biguanides?

A

liver and renal

289
Q

how does SGLT2 inhibitors work

A

increase glucose diuresis

290
Q

what is SGLT2

A

glucose transport in proximal nephron tubule to increase glucose reabsorption by the kidney

291
Q

whats the med for SGLT2

A

canagliflozin

292
Q

how does sulfonylureas work

A

increase insulin release and receptor sensitivity

293
Q

what is the med for sulfonylureas; duration, onset, peak

A

glyburide
duration 10-24 hr, PO
onset 1 hr
peak 2-3 hr

294
Q

what is the side effect of sulfonylureas

A

weight gain

295
Q

which population should avoid taking glyburide

296
Q

how does incretin enhancers work

A

stimulate insulin release

297
Q

what is incretin

A

hormone released from small intestine with food ingestion to stimulate insulin release

298
Q

what is the med for incretin enhancers; route

A

dulaglutide; Subcutanous injection

299
Q

what is glucovance

A

combination meds of glybruide and metformin (sulfonylureas to increase insulin release and biguanide to decrease glucose)

300
Q

glucose is triggered by

A

concentration of specific substances

301
Q

epinephrine is triggered by

A

neural stimulation

302
Q

aldosterone is triggered by

A

endocrine sequence

303
Q

most needy glucose system

A

nervous system (brain)

304
Q

functions of insulin

A

glucose cellular uptake
promotes storage formation
amino acid cellular uptake

305
Q

glucagon is synthesized in and when

A

alpha cells (opposite of insulin); low blood glucose

306
Q

glycogen is produced by

307
Q

somatostatin

A

inhibit insulin

308
Q

processes of insulin action

A

binds to tyrosine kinase (cellular membrane receptor) –> activates kinase enzyme within cell –> stimulate glucose transporter channels to open to glucose

309
Q

what lead to insulin secretion

A

glucose enters pancreatic beta cell via glucose transporter –> metabolized via glucokinase into ATP –> close K channels on beta cell –> depolarization –> insulin secretion

310
Q

glucocorticoids

A

utilize energy stores; gluconeogenesis

311
Q

catecholamines

A

stimulate glycogenolysis and lipolysis; gluconeogenesis

312
Q

growth hormone

A

long term stress= stimulate insulin secretion

313
Q

s/s of DM I

A

hyperglycemia, glycosuria, polyuria, polydipsia

314
Q

s/s of DM I when liver starts to metabolize fatty acid

A

ketonuria, changes in LOC, metabolic acidosis, coma, death

315
Q

s/e of DM I (systemic)

A

endothelial dysfunction, decreased angiogenesis, oxidative stress (retinopathy, neuropathy, nephropathy)

316
Q

type 1A DM I vs type 1B DM I

A

all Insulin dependent

1A: genetic predisposition and triggering event
1B: autoimmune

317
Q

fasting glucose normal

318
Q

basal insulin level

319
Q

peak insulin level

A

60-90IU/mL

320
Q

4 preparation types

A

rapid acting
long acting
short acting
intermediate acting

321
Q

administer insulin route

A

SC:
needle injection
portable pen injector
insulin pump

only IV if too ill

322
Q

unit for insulin

323
Q

rapid acting insulin

A

onest: 10-15 min
peak: 1-2 hr
meal time bolus (eat right away)

324
Q

meds for rapid acting insulin

A

humalog, novorapid, apidra, diasp (4 min onset)

325
Q

rapid acting insulin is used in

A

achieve boluses & customize basal insulin requirement

326
Q

long acting insulin

A

onset: 90 min
duration: up to 24 hrs

administer 1-2 x daily

327
Q

long acting insulin is used in

A

background, must have separate syringe for injection, never IV

328
Q

meds for long acting insulin

A

levemir, lantus, tresiba (ultra long >30hrs)

329
Q

short acting insulin (regular)

A

onset: 30 min
peak: 2-3 hr
duration: 6.5 hr

the only that can IV

330
Q

meds for short acting insulin

A

novolin ge toronto, humulin R, entuzity (5x more concentrated)

331
Q

which type of insulin to treat ketoacidosis; which route

A

short acting insulin; IV

332
Q

intermediate acting insulin

A

onset 1-3 hr
peak 5-8 hrs
duration: 18 hrs
monitor for night hypoglycemia

333
Q

meds for intermediate acting insulin

A

Humulin N, novolin ge NPH

334
Q

which type of insulin is best for patients who take steroids

A

intermediate acting insulin (can match sugar peaks)

335
Q

total daily insulin requirement

A

0.55U x patient weight (kg)

336
Q

1 IU= how many glucose and carbs

A

1.5-2.5 mmol/L of glucose

15g of carb

337
Q

what does BBIT stand for

A

basal
bolus
insulin
titrate

338
Q

how often do you monitor glucose level for patients taking insulin

A

4x per day minimum (pre meal 3x, bedtime)

8x for newly diagnosed patients(pre3x/post3x meals, bedtime, nighttime)

339
Q

when to take long acting insulin best to avoid night hypoglycemia

340
Q

which level of glucose is considered too high/low

341
Q

what is sliding scale

A

an outline of blood glucose levels & insulin dose

342
Q

s/s of hypoglycemia

A

rapid onset!!

nausea, diaphoresis, tachycardia, hungry, clumsiness, confusion, tingling around the mouth, nervousness, headache, shakiness, dizziness, sweat a lot

343
Q

s/s of hyperglycemia

A

thirsty, fatigue, weak, blurry vision, hungry, pee a lot

344
Q

treatment for hypoglycemia

A

glucose gel/tablet 15gx4, apple juice (conscious)

50% dextrose IV, glucagon IM (unconscious)

345
Q

treatment for hyperglycemia

A

insulin IV (regular, hydration, optimize both perfusion and potassium

346
Q

how is potassium in hyperglycemic patients

A

potassium shift out of cells

347
Q

s/s in DKA patients

A

Kussmaul breathing, LOC, fruity breath, ketones pee

348
Q

what regulate hunger

A

Ghrelin stimulates peristalsis + dopamine continues to stimulate appetite

349
Q

what regulate satiety

A

leptin, insulin, CCK+PYY

350
Q

what decrease hunger

A

sympathetic stimulation, low iron (Decrease ghrelin)

351
Q

Pax7+/Myf5+ stem cells

352
Q

Pax7-/Myf5- stem cells

353
Q

brown adipose tissue function

A

thermogenesis for insulation + synthesis

354
Q

white adipose tissue functions

A

energy storage: subcutaneous and visceral fat

355
Q

which population has the highest brown adipose tissue

356
Q

what metabolic effects do WAT have

A

leptin synthesis and regulation, adiponcectin synthesis and secretion, cytokines (growth factors)

357
Q

High WAT impact on leptin hormone

A
  1. leptin BBB distribution and receptor binding –> hunger signaling
  2. since leptin total levels are elevated –> cause inflammation

result: weight gain, arthritis, joint deformity, back pain

358
Q

function of adiponectin hormone

A 
suppress fatty acid influx into the liver (x fatty liver)
increase fatty acid breakdown
enhance insulin function
enhance glucose uptake
anti inflammatory
359
Q

High WAT impact on adiponectin

A

decrease in adiponectin synthesis and secretion, increase inflammation, insulin resistance, fatty acid deposition.

result: pro inflammatory diseases, cardiac diseases, cholecystitis, inflammation of galbladder

360
Q

High WAT impact on cytokine protein

A

increase level of cytokine

result: inflammatory disease, atheroscleosis, metabolic alternation leading to insulin resistance

361
Q

metabolic risk of being obese/develop DM

A

high estrogen, low testosterone, impaired thyroid function, rare metabolic diseases

large waist circumference, elevated BP, low plasma HDL, elevated plasma triglycerides and fasting plasma glucose

362
Q

firmicutes and bacteroidetes function

A

firmicute: higher absorption of calories
bacteroidetes: decrease absorption of calories

363
Q

how to increase beneficial GI bacteria

A

probiotics and dietary fiber

364
Q

pathology for obesity

A

gastric reflux, urinary incontinence, obstructive sleep apnea, impaired wound healing, depression, drug interaction (lipophillic drugs stay in body longer), pregnancy hypertension

365
Q

BMI for obesity

A

> 25

>40 morbid obesity

366
Q

weight circumference for normal male/female

A

102cm for male; 88cm in women

367
Q

skinfold measrement can be done in which areas

A

tricep, bicep, subscapula, suprailiac

368
Q

lipase inhibitor function and s/e

A

i.e. orlistat

med for obesity; decrease fat absorption in the intestine
s/e: decreased lipophilic medications absorption, pregnancy category X, GI bloating, fecal fat

369
Q

anorexiants function and s/e

A

i.e. contrave

med for obesity; act on brain to control appetite
s/e: CNS effect

370
Q

what is bariatric surgery?

A

surgery for obesity; (gastric bypass)

limit food absorption

371
Q

what is dumping syndrome? s/s

A

after bolus feeding; rapid transit of food into small intestine –> “high insulin release and sudden hypoglycemia”

abdominal cramps, hypoglycemia, N&V

372
Q

treatment for dumping syndrome

A

eat smaller amount of food, low sugar foods

373
Q

How is TSH synthesized? what does it produce?

A

thyroid stimulating hormone

hypothalamus releases TRH and trigger synthesis and release of TSH by anterior pituitary –> TSH activate thyroid glands to synthesize and release thyroid hormones (T3,T4)

374
Q

how is thyroid hormones produced

A

produced by follicular cells

after eaten iodide –> enter follicular cells –> converts to iodine atoms –> attach to tyrosine –> secrete

375
Q

T3 vs T4 and function

A

T3 = active form; increase ATP production therefore basal metabolic rate

376
Q

what is parenteral

A

IV, IM, SC

377
Q

How many calories per day are recommended as a rule, to meet basic metabolic demands?

A

10 cal/lb in an adult

378
Q

first drug of choice for ventricular fibrillation is and why

A

Epinephrine because it’s a non-selective sympathomimetic

379
Q

what is STEMI

A

total coronary artery occlusion infarct

ST elevation –> cant rest

380
Q

Beta Lactamase is an example of a bacterial enzyme, which causes drug-resistant ______________.

A

Penicillins

381
Q

What is the synergistic treatment if there is a likely resistance to Pencillins?

A

Clavulanic Acid; combined with penicillion = overcome antibiotic resistance

382
Q

What is the most likely side effect of Ca++ blockade in smooth muscle cells?

A

constipation

383
Q

morphine is

384
Q

common s/e in opoids

385
Q

How do Opioids work - mechanism of action? how to treat overdose?

A

Inhibit Substance P neurotransmitter; antagonist

386
Q

which drug class contains this drug: Aluminium Hydroxide? magnesium hydroxide? calcium carbonate

387
Q

How do NSAIDs work?

A

cyclooxygenase inhibition COX-2

388
Q

hypernatremia; hyponatremia

A

> 145;<135

389
Q

hyperkalemia;hypokalemia

Pharm Final Review (1 decks)

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