final Flashcards
three classes of antithrombotics
anticoagulants - decrease synthesis of coagulation factors / stop the coagulation cascade
antiplatlets
thrombolytics/fibrinolytics - dissolve thrombin/fibrin deposits at site of injury
heparin
anticoagulant - stimulates anti-thrombin and inhibits coagulation proteases
streptokinase, urokinase are which type of anti-thrombotics
thromolytic-
converts plasminogen to active form plasmin - degrades fibrin and dissolves the clot
streptokinase, urokinase
subtypes of anti-platelet drugs
- platelet aggregation inhibitors - aspirin and other COX inhibitors
- oral thienopyridines - inhibit ADP induced platlet aggregation - prasugrel
- glycoprotein platelet inhibitors - block glycoprotein IIn/IIIa receptors to reduce aggregation
- vorapaxar - PAR-1 (protease activated receptor) antagonist - can be used in combination with aspirin to reduce the likelihood of athero-thrombotoc events in patients with a history of MI
heparin vs warfarin
both are anti-coagulants, heparin administered parentally (injection), warfarin is oral
Heparin inhibits thrombin and fibrin (clotting agents)
warfarin is vitamin K antagonist
apolipoproteins
proteins in the plasma which facilitate the carriage of other lipids/cholesterol in the blood
seven classes of lipids
chylomicrons
chylomicron remnants
VLDL
VLDL remnants (IDL)
LDL
HDL
Lipoprotein a (Lp(a))
four major functions of apolipoproteins
1) scaffolding and structural support
2) guide the formation of lipoproteins
3) ligands for lipoproteins
4) activate and inhibit enzymes in the lipoprotein metabolism process
endogenous lipid pathway
begins with VLDL. converted to free fatty acids and IDL. then IDL to LDL which is taken up into the tissues (mostly the liver) and then reversible cholesterol transport to HDL
pro-atherogenic lipids (lead to atherosclerosis)
VLDL, IDL, LDL, Lipoprotein A, Apolipoprotein B 100 (the main structural protein of LDL)
which lipoprotein is anti-atherogenic
HDL (good cholesterol - H as in happy)
atherogenesis
the process of atherosclerotic plaque formation induced by inflammatory cytokines, ROS, and extracellular matrix proteins like metalloproteinases
Lp(a) is an independent risk factor for
atherosclerotic events
t/f - dyslipidemia can be the result a genetic disorder
true
hyperlipidemia
where the LDL, total cholesterol, triglyceride levels, or lipoprotein levels are higher than the 90th percentile of the population, or the HDL levels are lower than the 10th percentile
necrotic core of a thrombogenic plaque
made of dead smooth muscle cells, macrophages, foam cells formed by the phagocytosis of oxidized lipid molecules
which factor is most important in determining if you have dislipidemia
HDL concentration
- HDL less than the 10th percentile of general population = hyperlipidemia (because the LDL levels are elevated)
statins in high doses can be used to reduce the formation of these lipids
triglycerides and VLDL
what is the mechanism of action for statins to treat hyperlipidemia
inhibits HMG-CoA reductase which catalyzes HMG-CoA to mevalonate, which is the rate-limiting step in the synthesis of cholesterol
bile acid sequestrants (BAS) may be used to treat hyperlipidemia by reducing»_space;>
LDL levels
BAS method of action for hyperlipidemia
interrupt hepatic circulation of bile acids to reduce atherogenesis and cardiovascular events
because BAS require bulk administration to treat hyperlipidemia _____ side effects are common
GI side effects
nicotinic acids (niacin), also known as _____ are helpful to increase _____ while decreasing _____ (for hyperlipidemia_
niacin aka vitamin b is used to increase HDL while decreasing LDL and triglycerides and lipoprotein a
Ezetimibe is the most common non-statin drug used to reduce …. its method of action is
LDL levels, method of action is inhibition of intestinal cholesterol absorption
PCSK9 Monoclonal antibodies are used in hyperlipidemia to significantly reduce the levels of
Lp(a) and LDL
________ is an oligonucleotide used to treat homozygous familial hypercholesterolemia, its method of action is the inhibition of apopB synthesis which reduces the formation of VLDL
mipomersen
general goal of diuretics
increase the rate of urine flow (diuresis)
increase the rate of sodium excretion (natriuresis)
and
modify renal handling of cations to reduce excess body fluid
list the six main types of diuretics
inhibitors of carbonic anhydrase
loop diuretics
thiazides
renal epithelial sodium inhibitors (potassium-sparing)
antagonists of mineral corticoid receptors
osmotic diuretics
this diuretic works by blocking carbonic anhydrase in the proximal tubule lumen and cell (both membrane-bound and cytoplasmic forms) to stop sodium bicarbonate reabsorption
acetazolamide
by themselves, carbonic anhydrase inhibitors such as acetazolamide are not very effective at reducing edema, but combined with ____, they work well with added efficacy in the distal parts of the nephron
sodium absorption inhibitors
what is the major drawback of carbonic anhydrase inhibitors such as acetazolamide
metabolic acidosis
general mechanism of action of acetazolamide (carbonic anhydrase inhibitor) as a diuretic
Acetazolamide inhibits the enzyme carbonic anhydrase which acts in the proximal tubule to reabsorb sodium, bicarbonate, and chloride. inhibiting this enzyme increases the excretion of these ions, which increases the excretion of water as well. increased bicarbonate excretion increases blood acidity.
mannitol is what kind of diuretic
osmolarity diuretic
what is the mechanism of action of osmotic diuretics
they inhibit water reabsorption in the proximal tubule and loop of henle (so more water is excreted) and increase the excretion of almost all electrolytes, they also draw water out of intracellular compartments. They are freely filtered but not reabsorbed, their inert presence triggers the action
loop/high-ceiling diuretics
work in the ascending nephron limb to stop NaCl reabsorption (increase its excretion) - blocks the kidneys ability to concentrate urine
thiazides (hydrochlorothiazide) mechanism of action
inhibit the Na/Cl symporter in the distal tubule, cause reabsorption of Calcium, and cause direct vasodilation
thiazides have little effect on the increased excretion of sodium or chloride, instead they affect
potassium, calcium, and uric acid - increase excretion of all
do thiazides affect renal blood flow or tubuloglomerular feedback
thiazides do not affect renal blood flow and because they act on the distal tubule (do not act on macula densa cells) they do not greatly impact tubuloglomerular feedback
in addition to being a diuretic, thiazides are great for the treatment of
hypertension
what effects do loop diuretics have on extracellular fluid volume, blood viscosity, and renin release
they increase extracellular fluid volume
decrease blood viscosity
inhibit renin release
triamterene and amiloride are diuretics that work by inhibiting renal epithelial sodium channels. they are typically used to offset the actions of other diuretics. What is the classification of triamterene and amiloride
potassium-sparing diuretics - named for their anti-kaliuretic effects - they interfere with the sodium-potassium exchange in the late distal tubule by blocking the sodium channels so the negative potential difference in the lumen is decreased, as this is the driving force for potassium entry into the lumen, potassium entry also decreases so less potassium is excreted
what are the therapeutic uses of potassium sparing drugs
they decrease the risk of hypokalemia caused by other diuretics like loops or thiazide while also enhancing the diuretic and anti-hypertensive response
aerosolized amiloride is helpful in improving the mucociliary clearance of cystic fibrosis patients
amiloride is useful for lithium-induced nephrogenic diabetes
aldosterone/mineralcorticoid antagonist diuretics are another form of this type of diuretics
potassium-sparing (K+ sparing) diuretics
aldosterone antagonist diuretetics like spiralactone and eplerenone work by
blocking mineral corticoid receptors in the late distal tubule and collecting duct (which have high affinity for aldosterone) - this reduces potassium excretion while enhancing sodium and water excretion
where is aldosterone produced
the adrenal glands
which diuretic does not require access to the tubular lumen to induce diuresis
aldosterone/mineralcorticoid receptor antagonists
why does the diuretic spironolactone produce reproductive system side effects like menstrual irregularities, impotence, and gynecomastia
they have some affinity for progesterone and androgen receptors
therapeutic uses of mineralcorticoid receptor antagonists (spironolactone and eplerenone)
spironolactone used with thiazide or loop diuretics to treat edema and hypertension - especially good for those with liver cirrhosis
spironolactone used to treat primary hyperaldosteronism.
osmotic diuretics are particularly useful in treating this occular disease
glaucoma
what is diuretic braking and why does it happen
the gradual reduction of a patients response to a diuretic that occurs after receiving the first dose - reduction of response magnitude with each subsequent dose. occurs because renal compensatory mechanisms are triggered to ensure that sodium excretion is consistent with sodium intake
mechanisms of diuretic braking
activation of SNS and RAAS
hypertrophy of renal epithelial cells
increased expression of renal epithelial transporters
alterations of atrial natriuretic peptide
reduction of arterial blood pressure
what is diabetes
endocrine disease associated with absolute or relative insulin deficiency due to apoptosis and necrosis of pancreatic beta cells
Type 1 diabetes is caused by
autoimmune destruction of insulin producing beta cells - may also be referred to as insulin dependent diabetes
type 1 diabetes is categorized by
low insulin levles thorughout the disease course
presence of insulitis and beta-cell auto antibodies
presence of high levels of insulinoma antigen-2-autoantibodies and ketoacidosis
type 2 diabetes is caused by
the dysfunction of insulin receptor pathways involved in the signal transduction cascade
OR
dysfunctional insulin secretion by beta cells (in the chronic stages of the disease)
describe insulin levels as seen in type 2 diabetics
in the early stages of the disease, high insulin (hyperinsulinemia) is common, but then low insulin results in later stages
what is common to both T1DM and T2DM
persistent hyperglycemia (too much glucose) due to impaired insulin secretion or insulin functioning - leading to the production of advanced glycation end (AGE) products which cause oxidative stress, inflammation, necrosis, and apoptosis
which transporter incorporates glucose into beta cells
GLUT2
which tissues are GLUT1, GLUT2, and GLUT4 found in
GLUT1 - red blood cells and endothelial cells - useful for blood monitoring of glucose
GLUT2 - rena; tubular cells, hepatic cells, and pancreatic cells
GLUT4 - adipose tissue, skeletal muscles, and cardiac tissue - site of major glucose metabolism
normally, a modest increase of glucose triggers a ______ of plasma insulin
modest increase in glucose concentration should cause a big increase in plasma insulin concentration
compare the response to insulin of normal vs type 2 diabetics
the same maximum response (glucose transport levels) are reached but while controls reach this max response at around 5% receptor occupation, type 2 diabetics only reach it at much higher glucose concentrations. this occurs due to downregulation of insulin receptors and disrupted postreceptor signalling pathways
the number of insulin receptors present on a target cell is determined by which three factors
receptor synthesis
endocytosis of receptors
endocytosis by degradation
** what are the potential pathways of downstream insulin signal transduction cascades that could be defective or impaired to cause T2DM
1 - SH2 proteins bind and phosphorylate tyrosin groups on the insulin receptor (important for lipid metabolism)
2 - insulin receptor tyrosine-phosphorylates and activated different cytoplasmic proteins
3 - (MOST IMPORTANT) - insulin receptor phosphorylates the tyrosine residues of INSULIN-RECEPTOR SUBSTRATES (IRS)
explain the importance of IRS proteins and the signal cascade for T2DM
when insulin binds to its receptors, IRS proteins become phosphorylated which begins a cascade via activation of the SHC domain, leading to:
a PI-3-kinase pathway triggers the insertion of GLUT4 into the plasma membrane and enhances glycogen synthesis (two ways of lowering glucose levels)
protein phosphatase 1 (PP1) pathway (also triggered by IRS phosphorylation) also activates glycogen synthase
IRS phosphorylation is the link between insulin and the activation of the SHC domain
measurement of ____ indicates glucose levels over the past three months
Hemoglobin A1c (HbA1c)
primary treatment methods for type 1 and type 2 diabetes
1: insulin
2: modify lifestyle factors, oral hypoglycemics, insulin (in later stages)
drug therapies for diabetics
insulin
insulin secretagogues
biguanides
incretins
thiazolidinediones
alpha-glucosidase inhbitors
SGLT-2 inhibitors
three major sites of action of insulin
1 - liver - promotes storage of glucose as glycogen, lipogenesis, stimulates protein metabolism
2 - muscles - uptake of glucose via GLUT4, increase glucose metabolism, promotes synthesis of proteins
3 - adipose tissue - increase uptake of glucose via GLUT4, stimulates breakdown of glucose, promotes formation of triglycerides, induces synthesis of lipoprotein lipase
what is the basal-bolus insulin secretion technique
injection regimen made to mimic endogenous secretion of insulin
side effects of insulin injections
hypoglycemia - need to give sugar to correct
weight gain
lipo-dystrophy at injection site
describe the two classes of insulin secretagogues used for diabetes treatment
sulfonylureas (glyburide) - bind to SUR-1 receptor on beta cells to stimulate insulin release - should be avoided in patients with CV diseases and has CYP45- contradictions. - will stimulate insulin release regardless of glucose levels, risk of hypoglycemia
meglitinides (repaglinide) - also bind to a SUR-1 receptor to stimulate insulin release - more rapid onset with a shorter duration of action and less risk of hypoglycemia
which drug therapy is the first line of defense for T2DM and how does it work
biguanides (metformin) increase glucose uptake and cell sensitivity to insulin (increase activity of AMPK)
- reduce glycogenolysis and gluconeogenesis
what are the benefits of biguanides like metformin for T2DM
they do not cause weight gain, reduce risk of heart attack, and do not stimulate insulin release so they are unlikely to cause hypoglycemia (like many other drug therapies for diabetes do)
what are the two prototype incretin drugs for diabetes and what are their mechanisms of action
liraglutide (GLP-1 agonist) and sitagliptin (DPP-4 inhibitors)
GLP-1 agonists are injectables
DPP-4 inhibitors are pills - they stop DPP-4 from breaking down GLP-1 as quickly, and GLP-1 increases insulin release and decreases glucagon release
side effect profile of liraglutide (GLP-1 agonist) vs sitagliptin (DPP-4 inhibitors
both have a risk of hypoglycemia - but less so than with insulin or insulin secretagogues
both have the possibility for the rare side effect of pancreatic disease
liraglutide has more intense GI side effects - tachycardia,arrhythmias, and gall stones as well
DPP-4 plays a role in the immune system so it may cause upper respiratory tract or urinary tract infections
tirzepatide is a new incretin therapy for type 2 diabetes. its better because
it also is an agonist of GIP - not just GLP-1
describe the mechanism of action of thiazolidinediones (glitazones) for diabetes
they are PPAR-Y agonists. PPAR-y receptors regulate genes related to glucose and lipid metabolism. they increase insulin sensitivity, reduce hepatic production of glucose, reduce triglyceride production while increasing HDL
because they act on genes they take awhile to work
lots were withdrawn from market because they have bad side effect profiles - heart failure, edema, weight gain
how do alpha-glucosidase inhbitors (AGIs) work for diabetes
they inhibit the breakdown of carbohydrates into glucose to prevent glucose absorption
acarbose is the prototype for AGIs for diabetes. what are its side effects
GI side effects including gas becasue bacteria feed on the undigested carbs
low risk of hypoglycemia
what is unique about SGLT2 inhibitors to treat diabetes
they act on the nephron (inhinbit sodium glucose cotransporter-2 in the proximal tubule to stop glucose reabsorption) opposed to the GI tract. in non-diabetics, all filtered glucose is reabsorbed. the reduction of reabsorption increases glucose excretion, osmotic diuresis, reduces blood glucose and may induce weight loss and reduced bp
SGLT2 inhibitor prototype
empagliflozin
treatment objectives for asthma
relieve obstruction via bronchodilators
reduce inflammation via steroids
reduce stimuli for hyper-responsiveness (reduce allergic reactions)
there are no treatment options to fix the remodelling of the airways that occurs in asthma
bronchitis and emphysema are the two types of COPD. define them
bronchitis = airways leading to the lungs get inflamed and fill with mucus
emphysema = destruction of the tiny air sacs at the end of the airways
two main classes of drug therapies for COPD and asthma
bronchodilators (beta-2 agonists, antimuscarinics, methyxanthines)
corticosteroids
** which receptors regulate bronchial smooth muscle
sympathetic nervous system - beta 2 receptors induce bronchodilation
parasympathetic nervous system - muscarinic (M1,2,3) receptors induce bronchoconstriction
what is the issue with LABAs (long acting beta-2 agonists) for asthma
theyre good because they have a longer duration of action but chronic LABA use leads to downregulation of beta-2 receptors, rendering SABAs ineffective as rescue inhalers. In order to combat this, you need to use inhaled corticosteroids to reset beta-2 receptor concentration back to normal
atropine is the prototype anticholinergic, but why is it not ideal for asthma treatment
atropine is non-specific, so it has lots of side effects (CNS toxicity, tachycardia, increased viscosity of mucus secretion, impaired mucociliary clearance)
ideally, you only want to block the M3 receptor as this is the major contributor to bronchoconstriction
which are the modified anticholinergics for asthma (reduced systemic absorption) and what is their most common side effect
ipratropium as a short-acting muscarinic antagonist (SAMA)
tiotropium as a long-acting muscarinic antagonist (LAMA)
dry mouth - antagonists of muscarinic receptor M3 decreases salivation
what is the problem with using methylxanthines as bronchodilators
they have a narrow therapeutic index and lots of side effects - nausea, vomiting, increased gastric acid release, polyuria, insomnia, palpitations, headaches, cardiac arrhythmias
the mechanism of corticosteroids is not fully understood, but we know they..
act in the nucleus
promote expression of some genes (anti-inflammatory mediators - transactivation)
inhibit the expression of others (reduce expression of inflammatory mediators - trans-reperssion)
prototype systemic corticosteroid
prednisone - bad side effects - osteoporosis, fat redistribution, obesity, hyperglycemia
inhaled corticosteroids prototypes and side effects
budesonide, fluticasone - oral thrush and dysphonia (voice hoarseness)
most common combination therapy for COPD
Long-acting beta agonist (LABA) combined with a long-acting muscarinic antagonists (LAMA)
most common combination therapy for asthma
inhaled corticosteroid and long-acting beta agonist
major challenge in treating resp disorders
mode of delivery - inhalation is ideal but aerosol delivery ends up with less than 10% reaching the alveoli because of particle size and inhaler technique
while there is a lot of overlap in the drug therapies for asthma and COPD, COPD is also treated with ____ while asthma is not
antibiotics
mucolytics such as _____ have been used to treat Asthma, COPD, cystic fibrosis, and the common cold
N-actylcysteine (NAC)
PDE-4 inhibitors are useful in the treatment of Asthma and COPD for their _____ effect
anti-inflammatory
Roflumilast is a PDE-4 inhibitor used to treat severe COPD but its use is restricted because
it is administerd orally and thus has a lot of systemic side effects like diarrhea. nausea, loss of appetie, headache
what is zileuton used for and what is zileuton not used for
oral inhbitor of 5-lipoxygenase - treatment of chronic asthma in patients older than 12, usually combined with inhaled corticosteroids
not helpful for acute asthma attacks
montelukast and zafirlukast are used to
prevent and treat chronic asthma
oral admin
montelukast and zafirlukast mechanism of action
cysteinyl leukotriene receptor antagonists (where leukotrienes are eicosanoid inflammatory mediators) at the CysLT1 receptors only. Cysteinyl leukotrienes are important for eosionphil recruitment and airway remodeling in chronic asthma
most newer drugs in development for asthma are _____ what are the advantages/disadvantages
give an example
monoclonal antibodies
they are more selective (and possibly more effective with less toxicity)
however they cost a lot more, have to be injected, and may have more risk of immune reactions
ex - omalizumab
omalizumab for asthma
monoclonal antibody that prevents interaction with IgE to stop histamine and leukotriene release
mepolizumab for asthma
inhibits IL-5 - which activates B lymphocytes and eosinophils for their proliferation and differentiation - this IL-5 reduces eosinophil counts and therefore reduce inflammation
what is special about the prototype Dupilumab for asthma
it is a monoclonal antibody with more than one target - working on interleukins IL-4 and IL-13
dextromethorphan is a cough suppressant, but due to its side effects it is used as
a drug of abuse because it illicits hallucinations at high doses
NMDA-type glutamate receptor antagonist
guaifenesin for coughs
expectorants - for mucus cough - lighten secretions
cystic fibrosis
genetic condition causing excessive thick mucous due to defective CF transmembnrane conductance regulator gene causing impaired chloride secretion, sodium reabsorption, and water transport
two methods of treating cystic fibrosis
correct the misfolded protein or activate the CFTR in the cell membrane
what is renin
an enzyme secreted by the kidneys in response to low blood pressure
what are the three main pathways to regulate renin secretion
1 - increase in NaCl in macula densa cells of the distal tubule = decreased renin secretion (renin raises bp, so less renin = lower bp)
2 - baroreceptors on afferent arterioles detect raised bp - renin secretion decreased
3 - beta adrenergic activity increases renin secretion, so beta blockers decrease renin secretion
describe the relationship between obesity and hypertension
obesity and weight gain are risk factors for the development of hypertension but hypertension will not cause obesity
describe the old guidelines for the stages of hypertension and how they compare to the new guidelines
stage 1: 140-159/90-99
stage 2: over 160/100
new guidelines propose stage 1 at 130-139/80-89 which would classify a lot more younger people as being hypertensive and thus starting them on drugs unecessarily and double the prevalence of hypertension in canada,
what is the drug of first choice for hypertensive people under 55
ACE inhibitors or angiotensin II receptor blockers (ARB)
ACE inhibitors stop the conversion of ANG I to ANG II, where ANG II causes hypertensive effects
first choice anti-hypertensive for those 55 and up or of african/carribean descent
calcium channel blockers because ACE inhibitors may cause angioedema in african
beta blockers affect heart rate how
direct bradycardia
alpha1 receptor blockers and vasodilators are both used to treat hypertension. How do they affect heart rate?
reflex tachycardia
minoxidil is an antihypertensive that works by opening potassium channels to induce vascular smooth muscle vasodilation. however it is used off label for
hair growth, as hypertrichosis is a side effect
ACE inhibitors cause this side effect due to raised bradykinin levels
dry cough
what are the four classes of drugs for anti-arrythmics
calcium channel blockers
sodium channel blockers
potassium channel blockers
beta blockers
which type of cells (pace maker aka av node and sa node, or myocytes) depolarize spontaneously in the heart
pace maker cells (AV node, SA node) depolarize spontaneously because they have a more positive membrane potential of around -70
which ion current causes the spontaneous depolarization in pace maker cells
If current (non-selective cation channels) but largely it is the sodium entry which begins the depolarization in phase 4, but then the calcium entry causes rapid depolarization in phase 0
which ion channel causes rapid depolarization in phase 0 of pacemaker cells
calcium
which ion causes rapid depolarization in myocytes
sodium
the rate of current of this ion determines the heart rate conduction velocity in cardiac myocytes
sodium
physiological potassium serum range is very narrow so both can cause arrythmias how
hypokalemia acts like a potassium channel blocking drug - slowing K+ efflux prolongs the action potential duration causing arrythmias
hyperkalemia depolarizes the membrane and in extreme cases slows conduction to a stop (when K+ over 14 mM) because the resting membrane becomes more positive, disabling sodium channels
there are three classes of sodium channel blockers, class B - lidocaine is
use dependent block of both open and inactive sodium channels, making it good for ischemic myocardium but it may cause a lot of symptoms because of non-specificity - early warning sign is nystagmus
what is special about class c sodium channel blockers
they are very potent and cannot be used in patients with left ventricular function
what is special about the anti-arrythmic amiodarone
it is a class III anti-arrythmic so it is mainly classified as a potassium channel blocker but it actually works by all four mechanisms. it has a serious adverse side effect of pulmonary fibrosis
the anti-arrythmic sotalol, a potassium channel blocker causes this very serious cardiac side effect
torsades de pointes - ventricular tachycardia due to prolonged repolarization
potassium channel blockers for anti-arrythmics mainly work on (myocytes or pacemakers)
myocytes
which type of calcium channels to calcium channel blockers act on for arrythmias
L type calcium channels
calcium channel blockers (for arrythmias) mainly act on which cells
pacemakers to reduce calcium entry in phase 0, thus decreasing depolarization and slowing heart rate
main effect of sodium channel blockers for arrythmias
decrease conduction velocity
gastric acid secretion is mediated by
induction: GASTRIN (G cells of stomach antrum), ach, histamine
reduction: somatostain
secretion of stomach mucus is induced by
prostaglandins PGE2 and PGI2
which drug is most potent to reduce gastric acid secretion, and what is its downfall
proton pump inhibitors - theyre good because they act after only a couple days but they may cause hypergastrinemia or hypersecretion
misoprostol is a valuable drug for ulcers as it increases mucosal defense - what is special about it
inhibits acid secretion in a dose dependent manner and also stimulates mucin and bicarbonate secretion
however it is contraindicated in pregnancy because of severe uterine contractions
when treating atrial flutter, you should follow this order of drug treatment to protect the ventricles
atrial flutter is when too many impulses are reaching the AV node
first give a drug to reduce conduction in the AV node like beta blockers or calcium channel blockers, and then give a drug to reduce heart rate like sodium channel blockers
how
is chemotherapy induced nausea treated
mainly by 5-HT3 antagonists but these are only effective in acute phase. to treat the delayed phase, you have to use substance P antagonists
motion sickness nausea is treated by
anti-cholinergics (scopolamine) which block muscarinic receptors
sucralfate is used for gastric ulcers, what is its mechanism of action
polysaccharide that forms a protective viscous sticky polymer which adheres to epithelial cells and ulcer craters under acidic pH
what is the role of dopamine in the GI TRACT
it is inhibitory, increased dopamine means decreased motility
which drugs can stimulate peristalsis in the upper GI tract if there is dysmotility
serotonin 5-HT4 agonists and Dopamine D2 receptor antagonists
motilin is a peptide hormone in the upper GI tract which stimulates smooth muscle contraction. which common class of drugs stimulates motilin receptors causing contraction of the stomach and upper small intestine
macrolide antibiotics like erythromycin
what is the difference between laxatives and cathartics
laxatives evacuate already formed fecal matter from the rectum
cathartics evacuate unformed watery material from the entire colon - they are much more harsh
how to saline laxatives work and what their bad side effect is
they use magnesium or phosphate ions to help retain water osmotically - phosphate salts may cause nephro toxicity
how do stool wetting agents work to treat constipation and what is their bad side effect
they reduce the surface tension of stool or soften it - bit these oils can cause lipid pneumonitis and aspiration so you cannot take them before bed
methylnaltrexone is used to treat constipation induced by
opiods - works by blocking peripheral opiod mu receptors
what are the actions of bismuth
relieves nausea and cramping, treats H. pylori via antisecretory, anti-inflammatory, and anti-microbial actions. may cause black staining of tongue and stool
loperamide (opiod) can be used to treat this GI condition
diarrhea - acts on mu receptors
what is irritable bowel syndrome
constipation, diarrhea, or both at seperate time
irritiable bowel syndrome can be treated using this kind of antidepressants
tricyclic
difference between inflammatory bowel disease colitis and crohns
ulcerative colitis - inflammation of the mucosal layer
crohns - inflammation of any part of GI tracy
crucial drug for treatment of inflammatory bowel disease
mesalamine - inhibits many steps in the immune and inflammation process - but is has adverse effects due to sulfapyridine which may cause nephritis
ischemia is defined as an imbalance between
myocardial oxygen supply and demand
what is angina pectoris
the main symptom of ischemia - an uncomfortable sensation in the heart during physical activity that goes away when you stop moving
describe the relation between plaques and symptoms in stable, variant, unstable, and syndrome x ischemia
stable - there is a chronic pattern of transient ischemia in response to physical activity that goes away when you stop - plaques are fixed in position causing vasoconstriction
unstable - there is increased frequency and duration of angina symptoms produced by less exertion and at rest caused by disruption of the plaques leading to platelet aggregation, thrombus formation, and vasoconstriction
variant - angina at rest - there is no plaques just intense vasospasms which reduce oxygen supply
syndrome x - there are symptoms of angina during exertion but there are no atherosclerotic stenosis or other vascular abnormalties shown on angiograms
sublingual nitroglycerin is used to quickly
stop angina attacks
beta blockers may be used for ischemia, describe the intended demographics for selective vs nonselective
non-selective ones like propranolol may aggravate asthma as they may also cause bronchoconstriction
cardioselective ones like atenolol are thus better for those with lung conditions but the high doses needed to treat angina may make them lose their sensitivity
how do nitrates work to treat angina
they decrease the oxygen demand and induce vasodilation (which reduces the workload of the heart) by donating NO (aka endothelial derived relaxing factor)
what are the two classes of calcium channel blockers for angina
dihydropyridines - dilate vessels - amlodipine - may cause dizziness and flushing due to potent vasodilation
non-dihydropyridines - decrease oxygen demands, reduce contractile force, slow heart rate - verapamil
what is special about the calcium channel blocker verapamil for the treatment of cardiac ischemia
this non-dihydropyridine calcium channel blocker is useful in the treatment of variant angina - but it cannot be combined with beta blockers because it may cause severe bradycardia
how does ranolazine help with angina
improves your capacity to exercise and reduces frequency of angina attacks
are there surgical techniques for angina
revascularization
- percutaneous coronary intervention - balloon in the vessel
- bypass graft - CABG
what is the most common cause of heart failure
left ventricle malfunction
three causes for left ventricle failure
impaired contraction
increased afterload
impaired ventricular relaxation leading to inadequate filling
two classifications of heart failure
failure with preserved ejection fraction - aka diastolic dysfunction - when the ventricle cannot relax properly so they do not fill enough
with reduced ejection fraction - systolic dysfunction - the heart muscles are weaker and can no longer pump enough blood to the body
when there is left sided heart failure, blood pools where
in the pulmonary veins causing shortness of breath
inresponse to heart failure, your body undergoes which three neurohormonal responses
increases sympathetic nervous system - increase HR, contractility, and vasoconstriction
increased RAAS - increase renin secretion to increase bp
increased antidiuretic hormone - increase vascular volume to increase water volume - initially helpful but wears out the heart chronically
what are natriuretic peptides
beneficial peptides secreted during heart failure like atrial natriuretic peptide and BNP - cause sodium and water secretion, vasodilation
endothelial 1 is a potent vasoconstricter
