TEST 2 Flashcards
1
Q
In the Loop of Henle, ______% of NaCl gets reabsorbed at the ascending loop.
A
20%
remember that water follows solute.. so 20% of water will be PASSIVELY reabsorbed here
2
Q
Loop Diuretic work in the ________ loop in the Loop of Henle.
A
Ascending
3
Q
_________ diuretics work by preventing the reabsorption of 20% of solute.
A
Loop
4
Q
The Distal Convoluted Tubule is where _____% of NaCl is actively reabsorbed into the ECF.
A
10
remember that water follows solute.. so 10% of water will be PASSIVELY reabsorbed here.
5
Q
Diuretics that work at the distal convoluted tubule are _____ as effective as loop diurectics
A
half
6
Q
In the collecting ducts, you have ________ exchange pumps…
A
Sodium Potassium
7
Q
The collecting ducts are where _____% of NaCl is actively reabsorbed.
A
5
remember that water follows solute.. so 5% of water will be PASSIVELY reabsorbed here.
8
Q
__________ is the hormone that is a stimulant for the production of the sodium-potassium exchange pumps
A
Aldosterone
9
Q
What is ADH?
A
Anti Diuretic Hormone
10
Q
What does ADH do?
A
ADH is a hormone within the body that causes the membranes in the collecting ducts to be more permeable to water.
This allows free water to be pulled into the body and thus concentrates the urine.
This is independent of solute.
11
Q
When you are running a marathon, and your body needs to conserve free water ______ is released and it causes free water to be absorbed which darkens the urine.
A
ADH
12
Q
Diuretic therapy:
MOA- General diuretics prevent active NaCl reabsorption and by doing this, it will limit the _______ reabsorption of water through the concentration gradient.
A
Passive
13
Q
The degree of urine flow is directly proportional to the amount of NaCl reabsorption in line…so the Loop diuretics produce ____ urine than thiazide diuretics that work further down the line at the distal convoluted tubule.
A
more
they produce twice as much urine because 20% gets blocked here vs. 10% at the distal convoluted tubule
14
Q
True or False
Loop Diuretics are less powerful than Osmotic Diuretics
A
False.
Loops are first in line so they prevent 20% of NaCl reaborption
15
Q
The closer to the glomerulus the ______ powerful the diurectic is.
A
more
16
Q
The closer to the collecting duct the ______ powerful the diuretic is
A
less
17
Q
Name the 2 categories of Potassium Sparing Diuretics.
A
Aldosterone Antagonists and Non-Aldosterone Antagonists
18
Q
Loop Diuretics are the __________ effective Diuretics
A
Most
19
Q
What kind of diuretic is Furosemide?
Must know for test
A
Furosemide is a Loop Diuretic
Other loop diuretics are:
Ethacrynic Acid
Bumetamide
Torsemide
20
Q
What is the method of action of loop diuretics?
A
To prevent the active reabsorption of NaCl by 20% at the ascending loop of henle
21
Q
What are the Pharmacokinetics of loop diuretics?
A
they are available in various dosage forms- orally, IV, IM
Diuresis of a pill starts in about 60 minutes and IV startes in around 5 minutes
22
Q
Name the therapeutic uses for loop diuretics
A
more severe cases when greater fluid mobilization is needed such as: CHF fluid overload edema from hepatic and renal failure
23
Q
Name the only Non sulfa loop diuretic
A
Ethacrynic acid
24
Q
Dehydration symptoms (one ADRs of diuretics)
A
orthostasis dry mouth dizzy skin turger BUN ratio (normal 10-1) when it gets wider it means dehydrated thirst
25
ADR of loop diuretics
```
*****hypokalemia most dangerous
dehydration
hypernatremia
hypochloremia
Hypotention
```
26
Loops and Thiazides together can be dangerous
true or false
true
27
IV loop diuretics can cause damage to the ears
True or false
true
usually transient ototoxicity
can also increase blood suger
28
Hyperuricemia can be caused by loop diuretics. Why is this important
because it increases uric acid which can cause gout
29
Where do Thiazide and Thiazide like diuretics work and what percentage of sodium do they block from getting reabsorbed
they work at the distal convoluted tubule
they block 10% of sodium and water from being reabsorbed
30
What was the prototype for Thiazide and Thiazide like diuretics
used to treat Hypertension and edema
| initial drug of choice for HTN
31
ADR's for Thiazides
the same as loop diuretics except for it increased serum CALCIUM
```
*****hypokalemia most dangerous
dehydration
hypernatremia
hypochloremia
Hypotention
```
32
What is different about potassium sparing diuretics compared to loop or thiazides
they are diuretics that reduce potassium loss
33
How do potassium sparing diuretics work
Aldosterone Antagonists work by blocking the effects of aldosterone
the net effect is less sodium potassium pump production
they retain k and excrete Na
34
What are the therapeutic uses for Potassium sparing diuretics (aldosterone antagonists)
cirrosis of the liver
CHF
primary hyperaldosteronism
35
Name 2 aldosterone antagonists****
spironolactone (more hormonal)
eplerenone (less hormonal)
36
ADR's of Potassium sparing diuretics (aldosterone antagonists)
```
hyperkalemia
menstrual irregularities
deepening of the voice
excessive hair growth in girls
gynomastia in men
```
37
name 2 non-aldosterone antagonists
triamterene and amiloride
MOA- block sodium potassium pumps
USES- electrolyte benefits
38
Osmotic Diuretics: Prototype Mannitol
- have to have a filtered needle to administer because it will crystalize as it cools
1. Four Properties
A. filtered- small enough
B. Undergoes minimal reabsorption (stays in Nephron
C. Not Metabolized
D. Pharmacology innert (doesnt do anything)
- Kinetics: has to be IV
Theraputics: prophalaxis of renal failure
intracranial pressure
ADR's - can make third spacing worse
DEATH
39
beta 1 receptors
heart rate increases
contractility increases
sympathetic nervous system
40
alpha 1 receptors
CONSTRICTION of the arteries and veins which leads to increased afterload
Sympathetic Nervous system
41
Stimulation of muscarinic receptors
is part of the parasympathetic nervous system
Decreases HR and contractility
reduces cardiac output
42
lower the preload
lower the cardiac output
43
vasodilater
is an afterload reducer
44
heart rate
increased through the sympathetic nervous system + beta 1 receptors when stimulated -> increase in HR and Contractility
45
Myocardial contractility
the force of contraction of the ventricals - beta 1 vs. muscarinic stimulation + more stretch
46
cardiac afterload (arteries):
the force that the heart has to overcome to pump blood
the greatest determinant is arteriole vasoconstriction and vasodilation
47
Starlings law
force of ventricular contraction is proportional to the stretch
soggy boggy- ends up not pumping as well
the greater the stretch the greater the contraction
48
Cardiac preload (veins)
how much volume gets to the heart
reduced preload: over diuresis, dehydrated,vasodilater
49
natriuretic peptides
protectors of volume overload
50
Baroreceptors
pressure sensor- stimulates the sympathetic nervous system
51
alpha 1 receptors
cause constriction of both arteries and veins
decrease contractility HR
52
Atrial Natriuretic Peptide
released from stretching in the atria
53
Brain Natriuretic Peptide
released from stretching in the ventricals
54
C natriuretic Peptide
released from stretching in the veins and the arteries
55
Name 2 NON-DHP Calcium channel blockers
Verapamil and Diltiazem
56
What is the MOA of NON-DHP Calcium channel blockers
block calcuim channels on arterioles and on the heart
| works similar to a Beta Blocker
57
What are the effects of Verapamil?
dilation of peripheral arteries
dilation of coronary arteries (increases perfusion)
Blockade of CA+ channels at SA Node (reduces HR)
Bockade of CA+ channels at the AV node
Blockade of CA+ channels in the myocardial tissue (decreases contractility)
58
What is the effect of blocking the SA node
the SA node is the pacemaker of the heart so blocking it would reduce Heart Rate
59
What is the effect of blocking the AV node?
calcium influx increases conduction through the AV node, blocking this would cause a decrease in the rate of electrical conduction in the Heart
this is important in regards to arrhythmias such as a-fib or a-flutter.
60
What kind of effect does calcium entry have on the Myocardium?
positive inotropic effect (pumping ability)
so blocking it with calcium channel blockers causes a negative inotropic effect
61
calcium channels in general:
vascular smooth muscle: calcium channels regulate contraction. So actually when calcium goes down the calcium channels, it causes vasoconstriction.
Vasoconstriction causes BP to increase.
If we block the calcium channels it produces the opposite effect. (vasodilation) which makes BP go down.
This is especially true on the arterial side of our vasculature, which is afterload.
Blocking calcium channels on the heart produces the same effects as beta blockers. Decreased heart rate and decreased contractility.
62
Calcium Channel Blockers =
the number one class of BP medication in the country
63
Beta Blockers end in
LOL
64
If it ends in SIN, what class of medication is it
Alpha 1 Antagonist
65
What is afterload
the force that the heart has to overcome to pump blood to the body (systole)
Afterload = Arteries
66
What is preload
Preload is the blood filling the heart on diasole (resting Phase)
Preload = veins
67
What is SVR
Systemic Vascular Resistance
same as PVR - Peripheral Vascular Resistance
= Afterload
68
What are the two classes of calcium channel blockers?
Nondihydropyridine Calcium Channel Blockers
Dihydropyridine Calcium Channel Blockers
69
What is a couple of differences between Nondihydropyridine Calcium Channel Blockers
and
Dihydropyridine Calcium Channel Blockers
NON-DHP=
- blocks calcium channels on arteries and heart
- Causes constipation
- bradycardia
- Prophylaxis of migranes
DHP-
- No constipation
- Reflex tachycardia
- Immediate release causes MI
70
What is the formula for Arteriole Blood pressure
Arteriole BP= CO x PVR
71
What is the formula for determining Cardiac Output
CO= SV x HR
72
What are the therapeutic uses of Verapamil
Angina - Vasospastic and Exertional
HTN- Arterial Vasodilator, will lower BP by dilating arteries to reduce the pressure, and also compromising Cardiac Output
Cardiac Arrhythmias- especiall super ventricular tachycardic arrhythmias
Prophylaxis of migranes
73
What are the ADR's of Verapamil
```
*** Constipation
Headache
Edema
Gingival Hyperplasia
bradycardia
*** Partial or Complete AV Block
*** Exacerbate CHF
```
74
What is angina
when the supply of oxygen is receeded by the demand of oxygen.
75
What is Vasospastic Angina
where there is actually a spasm of the blood vessel
76
What is Excertional Angina
is where the supply of oxygen is exceeded by the demand.
for example- sprinting and feeling a burning sensation in your legs, if you slow down and walk, the burning goes away.
Same thing with your heart if you reduce the heart rate, the hear doesnt beat as hard, thus reducing your oxygen demand.
It is like pushing a piano without wheels on it, but if you put wheels on it, it is less difficult
77
All pure afterload reducers can cause:
Edema
| Headache
78
What are the contraindications for NON-DHP Verapamil and Diltiazem
2nd or 3rd degree heart block
| CHF
79
What are the drug interactions for NON-DHP Verapamil and Diltiazem
Digoxin- is a narrow therapeutic index drug that if added to verapamil NON-DHP can exacerbate bradycardia and lower HR way to much. Digoxin might need to be reduced by as much as 50% while taking Verapamil
Beta Blockers- causes profound supressant effects on the heart because NON-DHP verapamil has the same effects as a beta blocker (lowers HR and Contratility)
80
What are the effects of Diltiazem
essentially the same as Verapamil except causes less constipation
dilation of peripheral arteries
dilation of coronary arteries (increases perfusion)
Blockade of CA+ channels at SA Node (reduces HR)
Bockade of CA+ channels at the AV node
Blockade of CA+ channels in the myocardial tissue (decreases contractility)
```
ADR-
*** Constipation
Headache
Edema
Gingival Hyperplasia
bradycardia
*** Partial or Complete AV Block
*** Exacerbate CHF
```
81
Verapamil and Diltiazem are both ______ of CP450
inhibitors
this can cause other drugs to build up to toxic levels
82
Dihydropyridine Calcium Channel Blockers (DHP)
anything that ends in PINE
most common antihypertensive peripheral artery dilating class, not as much effect on the heart as NON-DHP
83
What is the DHP prototype
Nifedipine
84
What is the MOA of Nifedipine
Profound blockade of calcium channels in the arteries. This is a substantial afterload reducer. Has little to no effect on the heart so not going to use for heart issues such as A-Fib or A-flutter
85
What are the direct hemodynamic effects of Nifedipine
vasodilation and thus reduces SVR (PVR-Afterload)
Dilates coronary arteries somewhat, which may help coronary artery perfusion.
Helpful in Angina as well
86
What are the indirect hemodynamic effects of Nifedipine
by lowering BP significantly, they can trigger the Barrowreceptor reflex
Barroreceptors are little monitors in our blood vessels that protect us from shock, when BP drops significantly they kick in.
This is a sympathetic response (Norepi) Beta 1 ->alpha 1...stimulated HR and Vasoconstriction.
Primarily occurs with Immediate Relsease DHP only
Immediate relsease calcium channel blockers are now banned due to causes MI
87
What are the therapeutic uses of Nifedipine
Angina (vasospastic and excertional) - works by decreasing afterload
HTN (only in extended release forms)
88
What are the ADR's of Nifedipine
```
dizziness and Headache
**** Peripheral EDEMA
Gingival Hyperplasia
Reflex Tachycardia (more with immediate rel)
No consipation
Fast acting Linked to MI
```
89
Nifedipine Toxicity
if taken in excessive doses, it loses selectivity
lowers HR and contractility
Presents with heart block and Bradycardia
90
Basic Concepts of Vasodilators
Afterload reducers:
drugs that dilate resistance vessesls (Arteries)
cause a decrease in afterload (the force that the heart has to overcome to pump blood)
91
Basic Concepts of Vasodilators
Preload reducers:
Drugs that dilate capacitance vessels (veins)
Reduces the drive for blood to return to the heart, lowers BP by reducing Cardiac Output. (reduces ventricular filling)
70% of our blood is on the venous side
92
Side effects of Vasodilators
Posterial Hypotension (especiall with venodilators)
Reflex Tachycardia
Volume Expansion
Edema (especially with afterload reducers)
93
What is posterial Hypotension
a fall in BP brought on by moving from a sitting or lying postition to standing
Mostly in Elderly population
Referred to as Orthostasis
****First Dose Effect of SIN drugs
94
What is reflex Tachycardia
Occurs from dilation of arteries or veins through the barrow receptor reflex.
over time this can lead to volume expansion by reducing the blood flow to the kidneys which triggers the RAAS system resulting in Aldosterone release which causes retention of sodium and water
95
Hydralazine MOA
selective arterial vasodilator (pure afterload reducer)
Very Powerful direct acting arteriole vasodilator
96
What is unique about the metabolism of Hydralazine?
Metabolism: through acetalation (the ability to acetalate a drug is genetic) idiosyncratic effects (genetic predisposition)
Slow acetalator = low doses
Fast acetalator = high dose
97
What are the primary uses of Hydralazine
Hypertensive Crisis (IV)
Drug Resistant Hypertension
Heart Failure if combined with Isosorbide (which is a nitrate
98
What is drug resistant hypertension
when on three drugs to the max and blood pressure still sucks
99
What are the ADR's of Hydralazine
reflex tachycardia (barrorecptor reflex) fixed with beta blocker
volume expansion (use diuretic)
Systemic Lupus Erythematosus like syndrome
100
What causes reflex tachycardia
barroreceptor reflex
101
What causes volume explansion
aldosterone complments of barroreceptor reflex stimulating RAAS
102
Minoxodil MOA
more severe vasodilator. Effects Afterload
103
What is Minoxidil used for
severe hypertesion
104
What are the adverse effects of Minoxidil
volume expansion
reflex tachycardia
**hypertrichosis (hair growth)
Pericardial Effusion (Tamponade)
105
Sodium Nitroprusside MOA
Body's own natural Vasodilator, veno and arterial. Once in the body breaks down into Nitricoxide
This is a preload and afterload reducer
This is purely an IV med, very useful in ICU for HTN Emergency
106
Sodium Nitroprusside Toxcity
Thiocynate toxcity presents with hallucinations and psychotic behaviors. Similar to ICu psychosis, treatement is to reduce the medication slowly and discontinue
cannot abruptly discontinue
107
RAAS
When blood volume is low, juxtaglomerular cells in the kidneys activate their prorenin and secrete renin directly into circulation.
Plasma renin then carries out the conversion of angiotensinogen released by the liver to angiotensin I
Angiotensin I is subsequently converted to angiotensin II by the enzyme angiotensin-converting enzyme found in the lungs.
Angiotensin II is a potent vaso-active peptide that causes blood vessels to constrict, resulting in increased blood pressure.
Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex.
Aldosterone causes the tubules of the kidneys to increase the reabsorption of sodium and water into the blood. This increases the volume of fluid in the body, which also increases blood pressure.
108
The vast majority of CLINICAL hypertension is cause by clinical ________.
Inertia
Clinical inertia is when you have the knowledge about something and choose to ignore it.
In the US, 31-34% of BP patients are controlled
109
What is normal BP
< 120/80
110
What is pre-hypertension
120/80 to 139/89
111
What is stage 1 hypertension
140/90 to 159/99
112
What is stage 2 hypertension
greater than or equal to 160/100
113
What is ISH
Isolated Systolic Hypertension
When systolic pressure is 140mmHg or higher and diastolic pressure is less than 90 mmHg
classic in the agin population
past the age of 65 diastolic pressure drops and systolic increases due to athlerosclerosis
114
What are the two main types of hypertension?
Primary Hypertension
and
Secondary hypertension
115
What is primary hypertension
hypertension of aging
Essential Hypertension
Hypertension that has no identifiable cause
116
What is secondary hypertesion
elevation of blood pressure induced by an identifiable cause.
Cure is Possible
```
Caused by things such as:
Smoking
Obesity
Drug Users
SIADH
MAOI
Pheochromocytoma (adrenaline secreting tumor)
Hyperaldosteronism
Renal Artery Stenosis
Hyperthyroidism
Parahyperthyroidism
```
117
What do you use to persuade patients to control their hypertension?
The consequences of Hypertension
Silent Killer
```
CHF = Reduce by 50%
Stroke= Reduce By 35-40%
MI = Reduce by 20- 25%
```
Target end organ damage - kidney diasease and eye disease
118
If a person and 55 and does not have HTN yet, what are their changes of developing it?
90%
119
What is the treatment goal for hypertension
Goal for most < 140/90
Goal for Diabetes or Chronic Kidney disease <130/80
120
What is TLC
Therapeutic Lifestyle Changes
```
*** Weight loss #1 way to help BP
Sodium Resriction
DASH Diet
Alcohol Restriction
Excercise
```
Smoking Cessation is a cardiac risk factor
121
Can TLC be as effective as pharmacotherapy?
Yes and everyone gets TLC no matter what
122
What are the determinants of Blood Pressure
Arterial Pressure = CO x PVR
PVR, SVR, and Afterload are all the same thing
Every blood pressure medication lowers BP some how or some way through this process
123
How do preload reducers work?
by reducing cardiac output
124
Cardiac output =HR x SV is influenced (ehanced or reduced) by how hard or how fast the heart beats.
So as far as reducing CO,
Beta Blockers- reduce HR and Contractility
NON-DHP (verapamil and diltiazem) decrease HR and contractility too
Blood Volume- the greater the blood volume that gets to the heart, the greater the stretch. The greater the stretch, the greater the contraction. (preload)
Venous return- how much blood gets back to the heart, reducing this lowers BP (venodilators)
All of these things effect cardiac output
125
How is peripheral vascular resistance regulated
by arterial constriction
126
What systems regulate blood pressure
RAAS
Barroreceptor Reflex - prevents hypoperfusion, shock.
Is a sympathetic response- increases HR, causes vasoconstriction.
Never adjust blood pressure meds within 3-4 weeks because during this time you are fighting the barroreceptor reflex
127
What are the classes of antihypertensive medications
```
Alpha 2 agonists
Beta Blockers = LOL
Alpha 1 antagonist = SIN
Afterload Reducers
Diuretics
Ace Inhibitors = PRIL
ARB's = Sartans
Aldosterone Antagonists
```
128
Name an Alpha 2 Agonist
Clonadine
MOA slows Norepi release so norepi builds up
SNS says Whoa
Can cause:
rebound hypertension
drowiness
dry mouth
129
Reserpine moa
takes away the precursor molecule that makes norepi
norepi declines
ADR depression
130
What two beta blockers have Alpha 1 and Beta 1 blockade capabilities
Carvedilol and Labetalol
131
Name some alpha 1 antagonists
Tamsulosin (used in BPH)
Phentolamine (used in Pheo)
Prazosin
SIN DRUGS
MOA- preload and afterload reducers by blockade of Alpha 1
```
Uses:
Essential HTN,
Alpha 1 Agonist Toxicity,
****BPH
****Pheochromocytoma
Raynauds Disease
```
```
ADR's
Orthostasis
Reflex Tachycardia
Nasal Congestion
Inhibition of Ejaculation (retro Ejaculation)
Sodium and Water Retention
```
132
Beta Blockers (LOL)
- Decrease heart rate
- Decrease contractility
- Decrease electrical conduction through your heart
Used for patients who have an elevated HR, have HTN, and have arrithmias
side effects: could have heart failure
133
Vascular system is solely controlled by the
Sympathetic nervous system
134
Alpha 1
Vaso constriction
Alpha 1 blockade used for bph
135
Whoa receptor
Alpha 2
Shuts Down additional release of neurotransmitters
136
Beta 1
On heart.
Increases conduction, contraction, rate
137
Beta 2
Arteries. Dilation
Sympathetic
Lungs- cause bronchi dilation- albuterol
Liver- glycogen breakdown
Skeletal muscle- enhances contraction
138
Norepinephrine is
Recycled in the nerve terminal
Or broken down by monoaminoxydase
139
Name the afterload reducers
Minoxadil
Hydralazine
DHP (Arteriole Vasodilators)
ADR=
Pheripheral Edema
Reflex Tachycardia
Volume Expansion
140
What is SVR
Systemic Vascular Resistance
How dilated or constricted arteries or arterioles are
141
Name a loop diuretic
furosemide
Other loop diuretics are:
Ethacrynic Acid
Bumetamide
Torsemide
```
ADR
*****hypokalemia most dangerous
dehydration
hypernatremia
hypochloremia
Hypotention
```
142
What is the most common diuretic used to treat HTN
Thiazides
ADR's-
the same as loop diuretics except for it increased serum CALCIUM
```
*****hypokalemia most dangerous
dehydration
hypernatremia
hypochloremia
Hypotention
```
143
What is the main ADR difference between Loop diuretics and Thiazides?
Loops decrease serum calcium
Thiazides increase serum calcium
144
What class are PRIL's?
Ace Inhibitors
MOA- Reduces levels of Angiotension 2, Dilates arteries and veins. Preload and afterload reducer.
Lisinopril, Captropril
```
ADR-
Hypotension
HYPERKALEMIA
cough
angioedema
```
DRUG OF Choice for diabetic nephropathy and heart failure.
CONTRAINDICATED- Renal Artery Stenosis
CATEGORY X
145
Name the ARBS (Angiotension 2 Receptor Blockers)
SARTANS
Losartan and Telmisartan
MOA- Does not interfere with the production of of angiotension 2 just blocks the receptor site.
Use SARTAN when you have ACE Cough, possibly angioedema
ADR-
Hyperklemia
Can still cause cough
Can Still cause Angioedema
CATEGORY X
CONTRAINDICATED- Renal Artery Stenosis
146
Name the aldoserone antagonists
potassium sparing diuretics
Spironolactone and Eplerenone (less Hormonal)
MOA- selectively blocks aldosterone receptors, eliminate volume expansion
Uses-
HTN
HF NYC 3-4 (trophic agent)
ADR's Hypoklemia, Gynecomastia, Mentral Irregularity, Deep Womans Voice, Hairgrowth
147
True or False
Don't use Ace Inhibitors and Potassium Sparing diuretic together.
True
148
Angiotension 2 + Aldosterone =
causes heart to change shape which leads to heart failure
149
Where is renin produced
by juxtaglomerular cells (JG apparatus)
150
What triggers the release of renin
Decline in BP
Low blood Volume
reduced sodium plasma
reduction in renal perfusion ****
151
Aldosterone
sodium and water retention
potassium wasting
released dehydration, bleeding, shock
152
anything that lowers preload also lowers
cardiac output
153
Vasodilators reduce
afterload
154
vasoconstriction
increases afterload
155
what is the most important determinant of blood flow?
vessel diameter
156
volume expansion
increase in total body water. Can also be classified as isotonic, hypertonic, or hypotonic
157
Hypokalemia
when serum levels drop less than 3.5 Meq/L
Causes: acidotic state, diuretics, vomiting, diarrhea, laxative use,
Significance- weakness, paralysis, and arrhythmias
treatment give K
158
Hyperkalemia
greater than 5 Meq/L
Cuases: renal failure, excessive k administration, spironalactone and eplerinone
significance- arrhythmias, cardiac arrest
treatment: if the heart is irritated infuse calcium salt. insulin with D5W, Kxlate
159
What Class Causes the First Dose Effect?
Adrenergic Antagonists- Alpha 1 Blockers
Tamulosin
Phentolamine
Prazosin
SIN drugs
160
Propranolol
Non Selective Beta Blocker
Blocks beta 1 and Beta 2
```
Uses-
HTN
Angina
dysrhythmias
MI
Hyperthyroidism
Stage fright
Migraines
Pheochromocytoma Glaucoma
```
```
ADR's
Bradycardia
Decreased Cardiac Output
Heart Failure
AV Heart Block
Rebound Cardiac Excitation
Bronchoconstriction
Inhibition of Glycogenolysis
```
NOT GOOD FOR DIABETICS
161
Metroprolol
Specific Beta 1 Blocker
```
Uses-
HTN
Angina
dysrhythmias
MI
Hyperthyroidism
Stage fright
Migraines
Pheochromocytoma Glaucoma
```
```
ADR's
Bradycardia
Decreased Cardiac Output
Heart Failure
AV Heart Block
Rebound Cardiac Excitation
```
162
Carvedilol / Labetalol
Alpha 1 Beta 1 Blockade
preload afterload reducer
reduces HR and Contractility
163
Patients with Newly diagnosed essential hypertension, who do not have compelling indications should get what treatment?
TLC
Thiazide Diuretic
164
Patients who have been diagnosed with HTN but have other compelling indications such as:
Stable Angina or arrhythmia
Unstable Angina
S/P MI
Beta Blockers
165
Patients who have been diagnosed with HTN but have other compelling indications such as:
BPH
Diabetes
CHF
ISH
BPH (alpha 1 antagonists, SINS)
Diabetes (ACE Inhibitor, ARB)
CHF (BETA OR ACE or ARB)
ISH (Thiazide and DHP- PINE)
166
stage 1 HTN = ______ drugs
1
167
Stage 2 HTN = ______ drugs
2
168
Hypertensive Emergencies: Emergent?
```
Target end organ damage Present.
Headaches
Visual Changes
Chest Pain
Stroke
```
Lower asap with Nitroprusside drip IV MEDS ONLY
169
Hypertensive Emergencies: Urgent?
No target end organ damage present
lower bp slowly with oral medications within a 24-48 hour period
170
Chronic HTN during pregnancy leads to a
placental abruption
give methyldopa alpha 2 agonist
171
What are the two main causes of heart failure
Uncontrolled Chronic Hypertension
| MI
172
Which Neurohormonal Systems drive the remodeling changes to compensate for loss of heart function?
SNS
RAAS
173
Name the Signs and Symptoms of Heart Failure
```
Orthopnea
SOB
DOE
Fatigued at rest
Tachycardia
Cardiomegaly
Pulmonary Edema
Peripheral Edema
Hepatomegaly
JVD
Weight Gain *****
```
174
New York Heart Association
Class 1- HF no symptoms
Class 2 - Symptoms that worsen with exertion
Class 3- Minimal Exertion to get fatigued
Class 4- Symptoms at rest
flows in and out. Measures the "right now"
so a 3 can go back to a 1
175
American College of Cardiology
based on the progression of the disease
Stage A- best- pt is at risk for developing HF No Symptoms or structural disease
Stage B- Structural Damage but no symptoms (remodeling)
Stage C- worst- advanced Structural damage- symptoms even at rest
Never go backwards so once a C never go back to a B ect..
176
Aldosterone Antagonists Spironalactone and Eplerinone
increase life expectancy
NYC 3-4 symptoms
177
CARVEDILOL
protects against SNS overstimulation, protects against cardiac arrhythmia
has shown to improve Ejection Fraction, increase excercise tolerance, and slow the progression of HF. Reduces hospitalizations, prolong survival
178
Digoxin
can improve exercise intolerance, but does not improve their mortality rate or make you live longer. Try everything else then Digoxin
Positive ionitropic efects on the heart. makes the heart more efficient. Improves functional status, Decreases heart rate
179
Digoxin and Potassium relationship
If K is even a little bit low, it can cause Digoxin Toxicity. This drug is very sensitive to low K.
It causes Arrhythmias and is a very low therapeutic index drug
180
What would you see with Digoxin Toxicity
Bradycardia
Arrhythmias
GI: anorexia, nausea, vomiting
CNS: fatigue and visual disturbances
181
What is Digoxin's therapeutic Range
0.5 - 0.8 ng/ml
182
What are the drugs that interact with Digoxin
Diuretics- hypokalemia
ACE I / ARBS - increase potassium levels and decrease therapeutic effects of Digoxin
QUINIDINE / AMIODARONE / VERAPAMIL
183
Stage A drugs
Cease high risk behaviors
| Treat disease states that compound risks
184
Stage B drugs
Cease high risk behaviors
Treat disease states that compound risks
Add ACE I / ARB plus BETA Blocker
185
Stage C Drugs
ACE I / ARB
Diuretics
Digoxin
Isosorbide or Hydrolazine (to replace ACE/ARB)
```
Drugs to avoid stage C-
Dysrhythmic agents- cause death make worse
NONDHP
DHP ONLY Amlodipine and Felodipine
NSAIDS-- cause NA H2o retention
```
