Overall Review Flashcards
(389 cards)
1
Q
Intranasal (localized or systemic)
A
localized drug action CNS effect (preparation dependent)
2
Q
inhalation
A
can be systemic or localized
3
Q
facilitated diffusion and Active transport
A
hydrophilic, large, ionized
4
Q
factors affecting absorption
A
- molecular characteristics (charge, size, lipophilicity vs hydrophilicity)
- administration route
5
Q
Absorption and Distribution
A
lipophilic, small, and non-ionized
6
Q
Excretion
A
hydrophilic, ionized
7
Q
First Pass
A
PO –> hepatic vein –> systemic body
8
Q
Examples of first pass metabolism
A
morphine, meperidine, diazepam, midazolam, lidocaine, propranolol, ETOH
9
Q
Factors affecting distribution
A
- PPB
- size of tissue
- blood flow to the tissue
- molecular characteristics
10
Q
Albumin
A
acidic drug
11
Q
Alpha 1 acid glycoprotein
A
basic drug
12
Q
Highly bounded PPB Examples
A
Warfarin, NSAID, ibuprofen, naproxen, furosemide, digitoxin
13
Q
Blood brain barrier
A
selective transport
P-glycoprotein pump
14
Q
volume of distribution (Vd)
A
drug dose/ measured drug plasma concentration
15
Q
inactive drug to active metabolite
A
prodrug
ig. codeine
16
Q
active drug to active metabolite
A
toxic
17
Q
Phases of metabolism
A
phase I: hydrolysis, reduction, oxidation (Cytochrome P450 group)
polar metabolite: ionized, saturable
Phase II: conjugation, polarization
18
Q
Inhibitors of CYP 450 1A2
A
Ciprofloxacin (inhibit metabolism)
-decrease metabolism -> manage diarrhea symptoms
19
Q
Inducers of CYP 450 1A2
A
Barbituates
Cruciferous vegetables
Tobacco
(increased metabolism)
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
21
Q
what are the excretory organs?
A
kidney (primary), saliva, bile, lungs.
22
Q
3 factors affecting renal excretion
A
- molecular characteristics (PPB, Urinary pH, metabolized)
- renal function (young vs old)
- cardiac output (renal blood flow)
23
Q
first order kinetics
A
readily metabolized in the liver
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
25
creatinine
checks your kidney function by looking at the amount of creatinine in your urine and blood.
26
half-life
time at which drug has lost half its Cmax concentration
27
examples of narrow TI meds
warfarin
dignoxin
phenytoin
tacrolimus
28
partial agonist
lower efficacy
| eg. buprenorphine (less effect than opioid)
29
inverse agonist
bind to the agonist site but produce the opposite effect
eg. caffine (inhibit the effect of adenosine, which prompts GABA release to inhibit wakefulness)
30
antagonist
blocks the receptor site but NO efficacy
| e.g. naloxone (for opioid misuse)
31
Common overdose drugs examples
```
acetylsalicylic acid (aspirin)
acetaminophen (tylenol)
fentanyl
cocaine
benzodiazepines
alcohol
antidepressants
```
32
overdose procedure
```
airway
breathing
circulation (perfusion)
disability (dysfunction)
exposure
```
33
toxidromes
toxic syndromes and signs
34
acetylsalicylic acid
function: decrease platelet aggregation （一直失血)
```
confusion
tachycardia
tachypnea
hyperthermia
diaphoresis 發汗
vomiting
```
35
acetaminophen
```
abdominal pain
loss of appetite
nausea/vomiting
diaphoresis
somnolence 嗜睡
```
36
opioids
```
bradypnea/apnea
bradycardia
somnolence/coma
pupils constricted
itching (allergic response relating to inflammation)
```
37
cocaine (stimulant)
```
agitation, tremors
tachycardia
tachypnea
hyperthermia
diaphoresis
pupil dilated
```
tx: sedatives
38
adsorption
activated charcoal
binding of drug to decrease its absorption
e.g. tylenol poisoning, asa, benzodiazepines
39
ways to increase elimination
1. activated charcoal (GI)
2. urinary alkalization (renal) e.g. acidic aspirin poisoning give sodium bicarbonate
3. hemodialysis (renal)
40
Parietal cells and gastric chief cells synthesize and secrete
HCL acid / Pepsinogen --> pepsin (active)
41
How do endogenous organs be protected from gastric juice
foveolar cells have mucous and bicarbonate, bile and pancreatic bicarbonate
42
What's the pH of GI? and pH after HCO3?
1.5-3.5, to 7
43
HCI positive feedback
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
44
GERD pathophysiology (2)
1. weak lower esophageal sphincter
2. delayed gastric emptying
--> mucosal injury
45
GERD treatment (3)
1. decrease acidity
2. avoid irritants
3. fundoplication (tight pylorus)
46
PUD pathophysiology
failure of endogenous protection (cell junctions and mucous/bicarbonate layer)
--> mucosal erosion
47
Treatment for H pylori
amoxicillin
48
Where does H pylori present in?
present in both 90% duodenal and 75% gastric ulcers
49
ranitidine
cimetidine
famotidine
H2 receptor antagonists
50
antibiotics to treat PUD
amoxicillin
clarithromycin
metronidazole
51
pepto bismol 3 utilization
antiinfective
antiacid
antidiarrheal
52
large intestine synthesizes what vitamins
vitamin b and k
53
noninflammatory vs inflammatory acute diarrhea
< 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
54
first and second line c. difficile treatment
1st: flagyl (DNA)
2nd: vancomycin(cell wall)
55
what does atropine mean
stimulate sympathetic system and block parasympathetic system --> inhibit GI function
56
Three types of diarrhea
1. osmotic diarrhea
2. secretory diarrhea
3. inflammatory diarrhea
57
IBS
neurologic bowel disorder (diarrhea)
CNS dysregulation of normal motility
triggered by stress, anxiety, etc.
58
What is Hirschsprung disease
ganglion cells in large intestine wall dont develop before birth. --> constipation
59
Five types of laxatives
1. bulk forming
2. softeners
3. saline and osmotic
4. stimulants
5. miscellaneous
60
cathartics
evacuation of the bowel for procedure
61
where is the vomiting centre
medulla and outside of BBB
62
H1 antagonism (antihistamine)
reduce vestibular excitation (motion sickness)
dimenhydrinate: diphenhydramine + chlorotheophyline
meclizine (dramamine)
diclectin (pregnancy): doxylamine + pyridoxine hydrochloride (vitamin b6)
63
antimuscarinic anticholinergics and meds
reduce vestibular excitation (motion sickness)
scopolamine - transdermal patch
64
5HT3 antagonist and meds
purpose: visceral pain
ondansetron
65
D2 receptor antagonism
purpose: GI pain
phenothiazines
metoclopramide
prochlorperazine
s/e: sedation
66
CB1 & 2 agonism
purpose: chemotherapy
cannabinoids: THC and cannabidiol
stimulate GABA to inhibit sympathetic activity
67
Cannabinoids meds
Dronabinol
Cesamet
Nabilone
Cannibas
68
whats the percentage of body fluid
60%
69
percentage of intracellular fluid
40%
70
percentage of extracellular fluid
20%
71
What to do when GI bleeding
stop contributing meds like antiplatelet, anticoagulants, thrombolytics, NSAIDs
give fluids and blood transfusion
give proton pump inhibitor
72
Expected osmolality
275 to 295 mOsm/kgH20
73
Osmolality is dependent on
number of dissolved solutes
```
dehydration= higher = more solutes
over-hydration = lesser = less solutes
```
74
Tonicity focuses on
sodium and dextrose amount in IV fluid
75
albumin 5% fluid tonicity
isotonic in the bag and hypertonic in the body
76
D5 1/2 NS fluid tonicity
hypertonic in the bag and isotonic in the body (dextrose is quickly utilized
77
how much fluid is needed for maintenance?
35ml/kg/day of water (grown adult)
| 4/2/1 rule
78
how much glucose is needed to limit starvation ketosis
50-100g/day
79
NPO meaning
nothing by mouth
80
colloids
aka. plasma expanders
supply protein into ECF and stays in circulation
e.g. plasbumin, alburex
81
treatment for hypovolemic shock
colloids
82
NS 0.9% contents and side effects
154 mEq Na
154 mEq CI
isotonic
hypokalemia and no dextrose (lack energy)
83
what is #1 choice for resuscitation fluid?
NS 0.9% adults 500mL
84
Lactated Ringer content
more electrolytes
potassium 4mEq
Calcium 2.7 mEq
lactate 28mEq
85
LR is not suitable for which population? why?
children; too high electrolytes, high lactate
86
D5NS and D5LR tonicity
hypertonic
87
Dextran 40 tonicity
isotonic, but hypertonic in the body
88
D10W tonicity
hypertonic
89
D5 0.45% NS
hypertonic; osmolality = 405 mOsm/L
90
25% albumin tonicity and treatment
hypertonic; resuscitation to replace deficits (IV volume expander)
91
3% NaCl tonicity and treatment
hypertonic; head injury to lower ICP
92
what is the first choice for maintenance fluid for pediatrics
D5 0.45% NS (requires electrolytes and dextrose)
93
0.45% NS tonicity
hypotonic
94
D5W tonicity
hypotonic in body but isotonic in bag
95
3.3% dextrose, 0.3% sodium
hypotonic
96
D5 0.2% NS
hypotonic
97
Electrolytes balance is important for?
nerve conduction and water balance
98
common causes and treatment of
Hyponatremia
Hypernatremia
<135 mEq/L; diuretics; D5NS
| 145 mEq/L; kidney failure; diuretics
99
common causes and treatment of
Hypokalemia
Hyperkalemia
< 3.5 mEq/L; diuretics; KCL IV/PO
| >5 mEq/L; K+ sparing diuretics; Kayexalate
100
tx of diabetic ketoacidosis
hypotonic fluid
101
tx of hypernatremia
hypotonic fluid
102
tx of cerebral edema
hypertonic fluid
103
tx of severe hyponatremia
hypertonic fluid
104
tx for dehydration patients d/t vomiting and diarrhea
isotonic LR
105
preeclampsia
gestational HTN
106
causes of gestational HTN
inflammatory cytokine release due to endothelial changes
107
risk of gestational HTN
DIC, thrombocytopenia
108
decreased elasticity of vessels = _____ peripheral vascular resistance
increased
109
orthostatic hypotension
drop of SBP <20mmHg or DBP >10mmHg
120/80 normal --> 100/70
venous pooling, transient
110
treatment of orthostatic hypotension
adrenergic agonists
111
Mean arterial pressure
70-100mmHg
112
CO=
CO=SV x HR
113
CPP=
MAP - ICP
map: usually the same
ICP: increase
114
whats the treatment of HTN (ER)
nitric oxide (direct acting vasodilator)
115
Meds for nitric oxide; s/e
nipride and hydralazine
| syncope (fainting), hypotension due to reflex tachycardia
116
4 types of treatment for HTN
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)
117
whats is 1st line HTN treatment
diuretics
118
4 types of diuretics
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
119
Aldactazide is a combination of ___ and ___ and excellent ______ therapy for HTN
thiazide and k+ sparing combination; maintenance
120
side effects of diuretics and loop specifically
hyperglycemia; ototoxicity
121
in vasoconstriction, liver produces _____ in _____ and kidney produces ______ in response to low BP.
angiotensionogen in plasma
122
how does angiotensinogen converts to angiotensin I
by renin
123
what does adrenal cortex produce?
aldosterone (increase sodium reabsorption)
124
what lead to the production of aldosterone?
angiotensin II in plasma
125
decrease ventricular
decrease BP
126
decrease preload
decrease blood volume
127
angiotensin II binds to receptors
blood vessels and heart, adrenal cortex, kidneys
128
1st line drug in heart failure
angiotensin converting enzyme inhibitors --> vasodilate
129
meds: thiazide diuretic + angiotensin receptor blocker
Hyazaar HCT; Cosart-H
130
treatment of angina and arrhythmias
calcium channel blockers
131
two types of calcium channel blockers
1. vascular selective (smooth)
| 2. cardio selective (cardiac)
132
treatment of arrhythmia and atrial fibrillation
cardio selective calcium channel blockers and beta blockers
133
Verapamil and diltiazem
cardiac muscle
134
Nifedipine and amlodipine
smooth muscle
135
adverse effects of calcium channel blockers
reflex tachycardia, peripheral edema, dysrhythmias, heart failure, hypotension
136
ginseng
calcium channel antagonist
| = ca2+ influx blocked
137
alpha 1 receptors function
cause vasoconstriction
138
alpha 2 receptors function
cause vasoconstriction
139
beta 1 receptors function
increase cardiac activity (HR)
140
beta 2 receptors function
bronchodilation and vasodilation
| increased breakdown of glycogen to supply energy
141
specificity:
atenolol
propranolol
metoprolol
beta 1 vosodilation
| beta 1 and beta 2 antiarrhythmic (
142
what is the adrenergic antagonist meds for antiarrhythmic
propranolol
143
specificity:
Prazosin
Phentolamine
(alpha 1) – peripheral vasodilation
| (alpha) – peripheral vasodilation
144
lopressor HCT
diuretic (thiazide) and adrenergic antagonist
145
how does CNS alpha 2 adrenergic agonists work? what does it inhibit?
decreased in sympathetic tone by decreasing presynaptic ca levels --> inhibiting release of norepinephrine
146
whats the treatment for resistant HTN
CNS alpha 2 adrenergic agonist
147
what lead to endothelial cell damage (clotting)
1. mechanical stress
2. immune response
3. oxidative stress
148
Site of injury (high cholesterol level) produce ____
VCAM-1
149
VCAM-1 causes the migration of ____ beneath endothelium
circulating monocytes
150
how is free radical released and what does it impact?
monocytes differentiate into macrophages and produce oxidative stress; LDL
151
oxidized LDL become _____ after phagocytized by ______.
form cell; macrophage
152
what organ and enzyme produces cholesterol?
liver; HMG-CoA
153
drugs lowering lipids (inhibit cholesterol)
1. statins (decrease LDL)
2. niacin (increase HDL) --> increase clearance
3. fibrates (decreases VLDL) --> increase lipolysis and metabolism
154
what is the first line treatment for post MI (myocardial infarction)
statin
155
what lowering lipids med is ideal for low HDL
niacins
156
HMG CoA inhibitor
statins
157
side effects of statin
myopathy, CYP2C9 and CYP3A4 enzymes interactions
158
pregnancy category X interferes with
fetal CNS myelination
159
oxidative stress is caused by?
free radicals (reactive oxygen species)
160
what function does oxidative stress damage? what does it lead to?
insulin resistance; inflammation
161
what is formed in antioxidant
formation of water molecules
| e.g. grape
162
4 types of manifestation of atherosclerosis
1. narrowing of the vessel
2. vessel obstruction due to plaque
3. thrombosis
4. weakening of the vessel wall
163
differences between chronic and acute CAD
chronic: stable angina, thick fibrous plaque
acute: unstable angina, risk of MI when plaque rupture due to clotting, unstable plaque
164
4 release signals for aggregation
1. adenosine diphosphate (ADP)
2. thromboxane A2
3. Thrombin
4. Glycoprotein IIB/IIIa receptor activation (make platelet bind)
165
describe coagulation process
injured vessel stimulate factor X --> prothrombin activator -->
prothrombin to thrombin
fibrinogen to fibrin
166
thrombin function
1. converts fibrinogen to fibrin
2. activate factor XIII (13) --> loose to stabilized mesh)
3. enhances platelet aggregation
4. facilitates its own synthesis
167
what is essential to blood coagulation
thrombin
168
clotting treatment
1. antiplatelet
2. anticoagulant
3. thrombolytic
169
STEMI
ST too high, unable to rest (ventricular fibrillation problem)
170
ischemia
decreased blood flow = decreased O2 in the body
171
which intrinsic enzyme appear in plasma first at 3 hrs?
troponin
172
injury of myocardial cells can lead to leaking of _______.
intrinsic enzymes: troponin, creatine Kinease, myoglobin
173
isosorbide =
organic nitrates and osmotics diuretics
174
whats the 1st line acute intervention for angina
organic nitrates (3 tablets, 5 min apart)
175
CABG
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
how does antiplatelet work?
block thromboxane A2 and block ADP in degranulation
177
meds for antiplatelet
ASA
dipyridamole
aggrenox (combination of asa and dipyridamole)
clopidogrel
178
How does ASA work to treat clotting?
it blocks COX1 enzyme and therefore inhibit thromboxane production = decreased platelet aggregation
179
How does clopidogrel work to treat clotting?
it blocks ADP to decrease platelet adhesion
180
baby aspirin function and recommended doses
treat inflammation in blood vessel; 81mg adult and 10-15mg/kg pediatric
181
kawasaki syndrome treatment
common in children
| baby aspirin
182
how does anticoagulants work?
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
meds for anticoagulants
heparin
low molecular weight heparins (enoxaparin, dalteparin)
dabigatran
warfarin
184
how does heparin work to treat clotting?
inhibit thrombin
185
how does dabigatran work to treat clotting?
prodrug; block thrombin receptors and factor
186
how does warfarin work to treat clotting
inhibit hepatic formation of specific clotting factor (2,7,9,10)
187
how can heparin induced thrombocytopenia occur?
immune reaction when heparin antibodies bind to platelet factor 4 to activate platelet and produce a hypercoagulable state
tx: use LMWH
188
what to monitor for warfarin activity
prothrombin time
189
what to monitor for heparin activity
activated partial thromboplastin time
190
what to monitor for LMWH activity
anti factor Xa levels
191
what to monitor for bleeding risk activity
complete blood count
192
how does thrombolytics work
alteplase
reteplase
tissue plasminogen activator (tPa) allows plasminogen in bloodstream to convert to plasmin = clot (fibrin) lysis
193
5 risk factors of thrombosis
```
blood stasis (bedrest)
high estrogen (birth control)
smoking
blood clotting disorders (antithrombin III deficiency)
surgery
```
194
Deep vein thrombosis
occurs when a blood clot (thrombus) forms in one or more of the deep veins in your body, usually in your legs.
195
pulmonary embolism is caused by
DVT; life threatening
196
treatment of pulmonary embolism
prevention is the key (compressino stockings)
ER: thrombolytics
197
what are the 3 cushing triads for ICP?
hypertension, bradycardia and apnea
198
cerebral edema can lead to increased ____
ICP
199
differences b/w ischemia and hypoxia
Ischemia is insufficient blood flow to provide adequate oxygenation.
This leads to tissue hypoxia (reduced oxygen) or anoxia (absence of oxygen).
200
two types of cerebral edema; difference
vasogenic: increased permeability (blood brain barrier is disrupted)
cytotoxic: increased ICP
201
which type of cerebral edema is caused by head injury, hematoma, hemorrhage, CNS infection?
vasogenic
202
which type of cerebral edema is caused increased intracellular fluid shift?
cytotoxic
203
the most common CVA (stroke)
ischemic not hemorrhagic
| artery completely blocked
204
transient ischemic attack
angina of the brain because artery temporarily blocked
| 短暫性腦缺血發作
205
what are the treatments for TIA and CVA
```
thrombolytics within 3 hours since onset
carotid endarterectomy (move plaque from carotid artery)
angioplasty
antiplatelet
anticoagulant
```
206
the most common artery involved in stroke
Middle cerebral artery (limb and face) - part of circle of willis
207
dysarthria
weak muscle control
208
apraxia
moving the muscles needed in the correct order
209
dyslexia
impairment of reading
210
dysgraphia
impairment of writing
211
agnosia
inability to recognize and identify objects/persons
212
2 risk factors for hemorrhagic CVA
atriovenous malformation, aneurysm
213
treatment of hemorrhagic
white/red/platelet cell count decreased
stabilize, osmotic diuretics, hypertonic NS, optimize perfusion, surgical evacuation
214
treatment for cerebral edema
3% NS & mannitol
215
what is arteriovenous malformation (AVM)?
congenital defect in formation of cerebral vessels- lack capillary network
216
problem with AVM?
high pressure arterial flow enters venous vessels rapidly --> rupture (hemorrhage)
217
S&S of AVM?
steal blood flow from surrounding area --> ischemia --> slow onset neuro deficits
218
treatment of AVM
surgical clipping (removal), radiation (Gamma knife), embolization
219
3 locations aneurysm can present in
cerebral
aortic abdominal
throacic
220
which part of cerebral does aneurysm largely present in
circle of willis (subarachnoid hemorrhage)
221
treatment if aortic aneurysm ruptures
systemic bleed: give fluids
222
treatment if cerebral aneurysms ruptures
hemorrhagic CVA: surgery
223
treatment of cerebral aneurysm
coiling or flow diversion before ruptures (stent directs blood away from the aneurysm itself)
224
what are the interventional meds to prevent thrombus prophylaxis (prevention) post surgery
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
what med to give for people with high risk for clotting
heparin
226
risk factor for aortic aneurysm in elderly?
age: elastin is not synthesized
227
what is cardiac tamponade
extra fluid builds up
228
causes of cardiac tamponade
aortic aneurysm, cardiac rupture (MI), cardiac intervention, cardiac surgery, trauma
229
what is pericardiocentesis
evacuate fluid from heart by needle and catheter to drain
230
what is intracerebral
within cerebral lobes
231
causes of hematomas
ruptured cerebral aneurysm, AVM, hemorrhagic stroke due to head injury
232
two locations of hematoma?
epidural (skull and dural) and subdural (dural and subdural space)
233
what is a common cause of epidural hematoma
skull fracture injury
234
what is a common cause of subdural hematoma
venous tearing caused by injuries
235
treatment for hematoma
decrease ICP, evacuate, 3% NS, mannitol
236
how does cardiac tamponade lead to hypotension then HF?
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
sign and symptoms of cardiac tamponade
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
how does starling law apply to pulsus paradoxus?
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
what does adrenal medulla produce
catecholamines, adrenaline, noradrenaline
240
what does adrenal cortex produce
glucocorticoids (cortisol), aldosterone, androgens
241
s&s of repeated stress?
salt craving, hypoglycemia, hyponatremia, fatigue
242
what happen in repeated stress in body?
repeat secretion of cortisol --> depletion
243
which organ responds to level of cortisol
hypothalamus
244
why is keto diet bad
metabolic acidosis:
the liver breaks down fat into ketones --> blood becomes acid
normal blood pH: 7.35 to 7.45
245
chronic risks of ketogenic diet
increased LDL cholesterol, kidney stones, decreased growth hormones, renal damage, bone mineral loss
246
differences between primary and secondary pulmonary hypertension
primary: idiopathic, hereditary
secdonary: disease
247
heart failure definition
condition which decreases the heart's ability to pump enough blood
248
afterload vs preload
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
what is cor pulmonale
(pulmonary artery increases too much)
| condition that causes right sided heart failure
250
right heart failure vs left heart failure
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
what is the most common cause of heart failure?
low CO = hypotension
252
How does the body compensate for decreased cardiac output in cases of congestive heart failure?
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
what does compensation of HF lead to?
tachycardia and ventricular fibrillation
254
2 pharmacotherapeutics ways to treat HF?
1. decrease cardiac workload and increase O2 supply
(decrease HR, oxygenate, decrease pre/afterload
2. increase contractility
255
what are the treatment for HF?
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
how does cardiac glycoside work?
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
how does cardiac glycoside work?
block exit of Na and increase Ca in cells & decrease SA-AV node conduction to decrease HR
result: increased contractility and increased CO
258
how do you call the loading dose of digoxin? what to monitor
digitalization; narrow TI so monitor HR (apical pulse x 1 minutes)
259
what is the first sign of toxicity for digoxin? whats the antidote?
vomiting and nausea; digibind
260
how does Phosphodiesterase inhibitors work?
blocks enzyme phosphodiesterase to increase cAMP activity
result: increased contractility in myocardial cells & vasodilation
261
how does Phosphodiesterase inhibitors work?
blocks enzyme phosphodiesterase to increase cAMP activity
result: increased contractility in myocardial cells & vasodilation
262
viagra
Phosphodiesterase inhibitor to treat erectile dysfunction (increased blood flow)
263
what type of agent is adrenergic agonist
sympathomimetic agents
264
how does adrenergic agonists work
increase contractility, increase cardiac output, some vasodilation
265
dobutamine action
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
dobutamine action
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
dopamine HCL action
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
3 treatment for acute heart failure; how do they work
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
what is dilated cardiomyopathy
left ventricle camber is enlarged due to weakened heart muscle
270
risk factor for dilated cardiomyopathy
genetics, gender (male 20-50)
271
how to treat dilated cardiomyopathy
loop diuretics, direct acting vasodilators, b1 agonists, heart transplant
272
2 treatment for chronic heart failure
(longer acting)
1. cardiac glycosides
2. ACE/ARBs
273
how does arrhythmias affect cardiac rhythm? (3)
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
2 treatment for arrhythmias
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
3 treatments of supraventricular tachycardia
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
what med is used to treat bradycardia
Atropine
277
what meds are used to treat ventricular fibrillation/tachycardia
amiodarone (K channel blocker), lidocaine (Na channel blocker)
278
What type of diabetes is NIDDM
DM II
279
DM II
increased tissue resistance/insufficient production
pregnancy hormones
pancreatic disease
280
New rise in ____ in DM II
pediatric
281
how to treat DM II
lifestyle, oral antidiabetic agents, insulin
282
If dont treat DM II
diabetic ketoacidosis, Hyperosmolar hyperglycemic state (Dehydration)
283
Insulin and glucose treatment for DM II
antidiabetic agents
blood glucose: decrease overall blood glucose and increase cellular uptake (Biguanides, SGLT 2 inhibitors)
insulin: increase release and receptor sensitivity
284
why corticosteroids is bad for DM II
increase gluconeogenesis and lower insulin receptor affinity
285
Whats the first line therapy for DM II
biguanides
286
how does biguanides work
1. increase metabolism to reduce GI glucose absorption
| 2. alter mitochondrial activity to increase cell glucose uptake and insulin release
287
whats the med for biguanides; onset and peak
metformin
onset 2-3 hr
peak 10-16 hr
288
what organs function are important to assess for biguanides?
liver and renal
289
how does SGLT2 inhibitors work
increase glucose diuresis
290
what is SGLT2
glucose transport in proximal nephron tubule to increase glucose reabsorption by the kidney
291
whats the med for SGLT2
canagliflozin
292
how does sulfonylureas work
increase insulin release and receptor sensitivity
293
what is the med for sulfonylureas; duration, onset, peak
glyburide
duration 10-24 hr, PO
onset 1 hr
peak 2-3 hr
294
what is the side effect of sulfonylureas
weight gain
295
which population should avoid taking glyburide
elderly
296
how does incretin enhancers work
stimulate insulin release
297
what is incretin
hormone released from small intestine with food ingestion to stimulate insulin release
298
what is the med for incretin enhancers; route
dulaglutide; Subcutanous injection
299
what is glucovance
combination meds of glybruide and metformin (sulfonylureas to increase insulin release and biguanide to decrease glucose)
300
glucose is triggered by
concentration of specific substances
301
epinephrine is triggered by
neural stimulation
302
aldosterone is triggered by
endocrine sequence
303
most needy glucose system
nervous system (brain)
304
functions of insulin
glucose cellular uptake
promotes storage formation
amino acid cellular uptake
305
glucagon is synthesized in and when
alpha cells (opposite of insulin); low blood glucose
306
glycogen is produced by
liver
307
somatostatin
inhibit insulin
308
processes of insulin action
binds to tyrosine kinase (cellular membrane receptor) --> activates kinase enzyme within cell --> stimulate glucose transporter channels to open to glucose
309
what lead to insulin secretion
glucose enters pancreatic beta cell via glucose transporter --> metabolized via glucokinase into ATP --> close K channels on beta cell --> depolarization --> insulin secretion
310
glucocorticoids
utilize energy stores; gluconeogenesis
311
catecholamines
stimulate glycogenolysis and lipolysis; gluconeogenesis
312
growth hormone
long term stress= stimulate insulin secretion
313
s/s of DM I
hyperglycemia, glycosuria, polyuria, polydipsia
314
s/s of DM I when liver starts to metabolize fatty acid
ketonuria, changes in LOC, metabolic acidosis, coma, death
315
s/e of DM I (systemic)
endothelial dysfunction, decreased angiogenesis, oxidative stress (retinopathy, neuropathy, nephropathy)
316
type 1A DM I vs type 1B DM I
all Insulin dependent
1A: genetic predisposition and triggering event
1B: autoimmune
317
fasting glucose normal
4-8mmol/L
318
basal insulin level
5-15IU/mL
319
peak insulin level
60-90IU/mL
320
4 preparation types
rapid acting
long acting
short acting
intermediate acting
321
administer insulin route
SC:
needle injection
portable pen injector
insulin pump
only IV if too ill
322
unit for insulin
U
323
rapid acting insulin
onest: 10-15 min
peak: 1-2 hr
meal time bolus (eat right away)
324
meds for rapid acting insulin
humalog, novorapid, apidra, diasp (4 min onset)
325
rapid acting insulin is used in
achieve boluses & customize basal insulin requirement
326
long acting insulin
onset: 90 min
duration: up to 24 hrs
administer 1-2 x daily
327
long acting insulin is used in
background, must have separate syringe for injection, never IV
328
meds for long acting insulin
levemir, lantus, tresiba (ultra long >30hrs)
329
short acting insulin (regular)
onset: 30 min
peak: 2-3 hr
duration: 6.5 hr
the only that can IV
330
meds for short acting insulin
novolin ge toronto, humulin R, entuzity (5x more concentrated)
331
which type of insulin to treat ketoacidosis; which route
short acting insulin; IV
332
intermediate acting insulin
onset 1-3 hr
peak 5-8 hrs
duration: 18 hrs
monitor for night hypoglycemia
333
meds for intermediate acting insulin
Humulin N, novolin ge NPH
334
which type of insulin is best for patients who take steroids
intermediate acting insulin (can match sugar peaks)
335
total daily insulin requirement
0.55U x patient weight (kg)
336
1 IU= how many glucose and carbs
1.5-2.5 mmol/L of glucose
| 15g of carb
337
what does BBIT stand for
basal
bolus
insulin
titrate
338
how often do you monitor glucose level for patients taking insulin
4x per day minimum (pre meal 3x, bedtime)
8x for newly diagnosed patients(pre3x/post3x meals, bedtime, nighttime)
339
when to take long acting insulin best to avoid night hypoglycemia
A.M.
340
which level of glucose is considered too high/low
10;4
341
what is sliding scale
an outline of blood glucose levels & insulin dose
342
s/s of hypoglycemia
rapid onset!!
nausea, diaphoresis, tachycardia, hungry, clumsiness, confusion, tingling around the mouth, nervousness, headache, shakiness, dizziness, sweat a lot
343
s/s of hyperglycemia
thirsty, fatigue, weak, blurry vision, hungry, pee a lot
344
treatment for hypoglycemia
glucose gel/tablet 15gx4, apple juice (conscious)
50% dextrose IV, glucagon IM (unconscious)
345
treatment for hyperglycemia
insulin IV (regular, hydration, optimize both perfusion and potassium
346
how is potassium in hyperglycemic patients
potassium shift out of cells
347
s/s in DKA patients
Kussmaul breathing, LOC, fruity breath, ketones pee
348
what regulate hunger
Ghrelin stimulates peristalsis + dopamine continues to stimulate appetite
349
what regulate satiety
leptin, insulin, CCK+PYY
350
what decrease hunger
sympathetic stimulation, low iron (Decrease ghrelin)
351
Pax7+/Myf5+ stem cells
BAT
352
Pax7-/Myf5- stem cells
WAT
353
brown adipose tissue function
thermogenesis for insulation + synthesis
354
white adipose tissue functions
energy storage: subcutaneous and visceral fat
355
which population has the highest brown adipose tissue
infants
356
what metabolic effects do WAT have
leptin synthesis and regulation, adiponcectin synthesis and secretion, cytokines (growth factors)
357
High WAT impact on leptin hormone
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
function of adiponectin hormone
```
suppress fatty acid influx into the liver (x fatty liver)
increase fatty acid breakdown
enhance insulin function
enhance glucose uptake
anti inflammatory
```
359
High WAT impact on adiponectin
decrease in adiponectin synthesis and secretion, increase inflammation, insulin resistance, fatty acid deposition.
result: pro inflammatory diseases, cardiac diseases, cholecystitis, inflammation of galbladder
360
High WAT impact on cytokine protein
increase level of cytokine
result: inflammatory disease, atheroscleosis, metabolic alternation leading to insulin resistance
361
metabolic risk of being obese/develop DM
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
firmicutes and bacteroidetes function
firmicute: higher absorption of calories
bacteroidetes: decrease absorption of calories
363
how to increase beneficial GI bacteria
probiotics and dietary fiber
364
pathology for obesity
gastric reflux, urinary incontinence, obstructive sleep apnea, impaired wound healing, depression, drug interaction (lipophillic drugs stay in body longer), pregnancy hypertension
365
BMI for obesity
>25
| >40 morbid obesity
366
weight circumference for normal male/female
102cm for male; 88cm in women
367
skinfold measrement can be done in which areas
tricep, bicep, subscapula, suprailiac
368
lipase inhibitor function and s/e
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
anorexiants function and s/e
i.e. contrave
med for obesity; act on brain to control appetite
s/e: CNS effect
370
what is bariatric surgery?
surgery for obesity; (gastric bypass)
| limit food absorption
371
what is dumping syndrome? s/s
after bolus feeding; rapid transit of food into small intestine --> "high insulin release and sudden hypoglycemia"
abdominal cramps, hypoglycemia, N&V
372
treatment for dumping syndrome
eat smaller amount of food, low sugar foods
373
How is TSH synthesized? what does it produce?
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
how is thyroid hormones produced
produced by follicular cells
after eaten iodide --> enter follicular cells --> converts to iodine atoms --> attach to tyrosine --> secrete
375
T3 vs T4 and function
T3 = active form; increase ATP production therefore basal metabolic rate
376
what is parenteral
IV, IM, SC
377
How many calories per day are recommended as a rule, to meet basic metabolic demands?
10 cal/lb in an adult
378
first drug of choice for ventricular fibrillation is and why
Epinephrine because it's a non-selective sympathomimetic
379
what is STEMI
total coronary artery occlusion infarct
ST elevation --> cant rest
380
Beta Lactamase is an example of a bacterial enzyme, which causes drug-resistant ______________.
Penicillins
381
What is the synergistic treatment if there is a likely resistance to Pencillins?
Clavulanic Acid; combined with penicillion = overcome antibiotic resistance
382
What is the most likely side effect of Ca++ blockade in smooth muscle cells?
constipation
383
morphine is
opoids
384
common s/e in opoids
itching
385
How do Opioids work - mechanism of action? how to treat overdose?
Inhibit Substance P neurotransmitter; antagonist
386
which drug class contains this drug: Aluminium Hydroxide? magnesium hydroxide? calcium carbonate
antacids
387
How do NSAIDs work?
cyclooxygenase inhibition COX-2
388
hypernatremia; hyponatremia
>145;<135
389
hyperkalemia;hypokalemia
>5;<3.5
