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First dose very low in patients with increased plasma renin activity
P- not given in Pregnancy
R- they produce rashes
The I IS FOR increased potassium level and increased renin levels
L is for low aldosterone and angiotensin II levels
ARBS- LOSARTAN, valsartan and candesartan- they directly block
angiotensin II receptors so these receptors do no work on arteriole or
venule receptors
Typically the angiotensin II binds to angiotensin 2 receptor on zona
glomerulosa and this allows the zona glomerulosa to release
aldosterone so when this receptor is inhibited this doesnt happen
Metoprolol and carvidolol are beta blockers used in CHF, carvidilol
blocks alpha and beta receptors (Beta 1 and beta 2)
Carvidilol is a alpha receptor blocker and non selective beta blockers
Blockage of alpha 1 receptor it produces the arteriole and venodilation
At the same time B1 receptor blockage reduces heart rate and B2
blockage reduces renin production
There are two types of cardiac heart failure- high output and low
output heart failure
Low output heart failure is present as a result of ischemic heart not
being able to produce the normal cardiac output 5L/min
The heart is failing to reach the demands of the peripheral tissue but
the main cause is reduced cardiac output
Hyperthyroidism- increases the metabolism of body, so oxygen
demand of tissues is increased so the heart to produce more CO to
meet the demands of these tissues
There is RVF, LVF and BVF
When there is LVF there is an increase in heart pressure on the left side
that backs up to the pulmonary capillary causing them to leak and
produce pulmonary edema
Clinically patients come with dyspnea, orthopnea or paraoxysmal
dyspnea
RVF- back pressure increase in right increase in atrium, so systemic
capillaries leak and patient develop generalized edema
LVF- pulmonary edema
RVF- generalized or systemic edema
BVF- congestion of pulmonary and systemic failure- Congestive heart
failure
Forward failure and backward failure also- when there is left ventricular
failure the heart cant pump well so there will be reduced cardiac
output and there is backward pressure increase leading to pulmonary
edema
Forward failure features- fatigueness, exercise tolerance is reduced
Backward failure- pulmonary edema cough, dyspnea, orthopnea and
paraxymal dyspnea
Pulse is weak forward failure
Cant breathe- backward failure
Systolic failure and diastolic failure- the difference is during diastoleleft ventricle relaxes for ventricular filling and accumulate proper EDV
Systolic function is it has to contract and so that cardiac output has to
be maintained, related to SV and EF
If the heart has infiltrative disease, suppose amyloid proteins deposited
into the myocardium and the ventricle thickens the thick wall cant
relax well- during the diastole it cant accommodate much blood
Very sever LV hypertrophy- stiff and cant relax in diastole, and
accommodate not a lot of EDV
Diastolic function failure and backward failure
If the heart is very much dilated and there is lack of systole- systolic
dysfunction and forward failure pronounced
Positive inotropic
Chronotrophic effect- HR, epine increases HR,
Chronotropic drugs are working on SA node
Clinotrophic effect
Dromotropic effect- conduction velocity- fast conduction from sa TO av
node we say positive dromotropic
Epinephrine has positive dromotropic action but ca channel blockers
slows it down
Coagulation pathway
Cancer drugs
Side effects:
NeurotoxicitySIADH vincristine
Coma- Ifosfamide
Cerebral toxicity
Cytosobine
Ototoxic + Kidney + N/V : cisplastin
To prevent cisplastin- water with saline and give a diuretic such as
mannitol
Alkylating agents- attach alkyl groups to DNA, allows cross linking of
base pairs and non specific
Typical alkylating agents- cyclophosphamide, ifosfamide, melphalan,
busulfan, mechlorethamine, chlorambucil, thiotepa
Side effects- myelosuppression, N/V, secondary malignancies,
hemorrhagic cystitis
Atypical alkylating agents- platinum compounds covalently bind purine
bases- cisplastin- nephrotoxicity and N/V
Carboplatin thrombocytopenia
Oxaliplatin cold sensitivity
All cause peripheral neuropathies, paresthesia
Nitrosureas- carmustine pulmonary toxicity, phlebitis, CNS
Antimetabolites
Inhibit DNA replication
Specific to S phase
Inhibit DNA replication or repair by mimicking cell compounds
S phase specific
Folate inhibitor: methotrexate inhibits DHF prevents regeneration of
THF
Adjuvant leucovorin and protects the healthy cells
Side effects- mucositis, myelosuppresion
Pyrimidine inhibitors- 5-FU
It inhits thymidylate synthetase
Bolus dose causes myelosuppression
GI prblems- mucositis, diarrhea
Leucovorin potentiate the action
Capecitabine- oral prodrug for 5-FU
Hand and foot syndrome palms and hand and feet become red and
blistering
Cholinergic Drugs
Direct acting and indirect acting cholinergic drugs
The peripheral nervous system is subdivided into the efferent and
afferent divisions
The efferent neurons signals away from the brain and spinal cord to the
peripheral tissues
Afferent neurons bring info from the periphery to the CNS
Afferent neurons provide input to modulate the function of the efferent
division through reflex arcs
CN III, VII, IX, X -> S2 to S4 of the spinal cord and synapse in ganglia
near or on the effector organs
The vagus nerve accounts for 90% of preganglionic parasympathetic
fibers in the body, postganglionic neurons from the nerve innervate
most of the organs in the thoracic and abdominal cavity
Effects of stimulation output is to increase the heart rate and BP,
mobilize energy stores of the body and to increase blood flow to
skeletal muscles and the heart while diverting flow from the skin and
internal organs
Dilation of pupils and bronchioles
Contraction of iris radial muscle pupil dilates
Contraction of iris sphincter muscle- pupil contracts
Contraction of ciliary muscle- lens accommodates for near vision
Kidney- secretion of renin (Beta 1 increases, alpa 1 decreases)
Uterus- relaxation of detrusor; contraction of trigone and sphincter
Parasympathetic stimulation- contraction of detrusor, relaxation of
trigone and sphincter
Gentalia stimulation of ejaculation
Stiumulation of erection
Stimulation of tears
Thick viscous secretion
Copious watery secretion
Increased rate; increased contractility
Decreased rate; decreased contractility
It is a potent bronchodilator
It is useful in av block
Dopamine it occurs naturally in the norepinephrine
Dopamine dilates renal and splanchnic arterioles by activating
dopaminergic receptors
It is the drug of choice for cardiogenic and septic shock and is given in
continuous infusion
Dopamine is the drug of choice for cardiogenic and septic shock--- it
raises BP by stimulating the beta receptors on the heart to increase
cardiac output and alpha receptors on blood vessels to increase total
peripheral resistance
It enhances perfusion to the kidney and splanchnic areas
Phenylephrine is direct acting synthetic adrenergic drug that binds
primarily to alpha 1 receptors
It has both systolic and diastolic blood pressures
It has no effect on the heart itself but rather induces reflex bradycardia
when given parenterally
Phenylephrine has replaced pseudoephedrine in many oral
decongestants
Beta 2 receptor mediated inhibition of degranulation of mast cells,
which prevents the release of histamine and other inflammatory
agents
Epinephrine is often used together with local anesthetics to prolong the
action of the anesthetic
This increased duration is due to the epinephrine induced
vasoconstriction (mediated by alpha 1 receptor activation) which
localizes the anesthetic at the desired site, slowing its systemic
distribution
The most appropriate management of cardiac arrest induced by
ventricular fibrillation is 200 J defibrillation
Additional shocks at higher energy should be given in case of initial
failure
If ventricular fibrillation persists the aha indicates that epinephrine
should be given
Norepinephrine causes an increase in systolic and diastolic pressure
and a concomitant decrease in heart rate
This pattern suggests that the decrease in heart rate is reflex vagal
discharge