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Glossary of Content fall 2010

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These vasodilators do not raise bradykinin levels and therefore rarely cause cough or angioedema
ARBs
True or false: Angiotensin II is a vasodilator
False
Blocking of COX-3 in the brain causes decreased levels of these
Prostaglandins especially E2
Acetaminophen overdose should be treated with and why:
acetylcysteine because it provides HS radicals that can neutralize the toxic metabolites
Acetaminophen causes fatal hepatic centrilobular overdose due to:
Glutathione depletion
Besides hepatotoxicity high doses of acetaminophen can cause:
Acute renal tubular necrosis (nephrotoxicity)
What does APAP stand for?
Acetaminophen
-AntiPain and AntiPyretic
-Chemical name is N-acetyl-Para-AminoPhenol

Acetaminophen is a weak inhibitor of what receptors
COX-1 and COX-2
AT1 is what type of receptor
Gq which means binding of Angiotensin II causes activation of PLC and increased Ca2+ release from the sarcoplasmic reticulum.
Binding of Ca2+ to what activates Myosin light chain kinase?
Calmodulin
True or false: the vasodilatory effects of ACEIs are equal to both arteries and veins
True
True or false: following treatment with ACEIs, there is reflex sympathetic activation
False
Name the major uses of ACEIs and ARBs
HTN, CHF, all stages of left ventricular failure especially following an MI, diabetic nephropathy
Use of antacids while taking ACEIs can cause:
Decreased bioavailability
ACEIs and ARBs increase or decrease excretion of K+
Decrease; do not need to give K+ supplement or K+ sparing diuretic with them
NSAIDs taking concurrently with ACEIs can cause and why:
Decreased antihypertensive effects due to decreased levels of prostaglandins
Drugs that are ARBs typically end in
-SARTAN
True or false: ACEIs and ARBs can be taken during pregnancy
False; potentially cause fetopathy, especially in the 2nd and 3rd trimesters
ACEIs are typically safe for patients with renal problems except those with:
Bilateral renal artery stenosis, can cause renal failure
The MOA of statins is
Inhibition of HMG:CoA reductase
Name the effects of HMG-CoA reductase inhibition
1.Decreased synthesis of cholesterol in the liver
2. LDL receptor upregulated expression and downregulated clearance so increased uptake of LDL
3. Possibly decreased VLDL synthesis due to decreased cholesterol

Clinical uses of statins are
Hypercholesterolemia (Type IIa)

The statin that is not a P450 substrate is
Pravastatin
The P450 substrates associated with statins are
3A4 and 2C9
The major side effects of statins are
Hypersensitivity
Hepatic enzyme elevation and dysfunction (see increased aminotransferase)
Rhabdomyolysis (increased creatinine and/or myoglobins)

HMG-CoA reductase blocks the conversion of HMG-CoA to
Mevalonate
One action of statins is vasoprotection due to
Serving as an antioxidant or anti-inflammatory agent on blood vessels
Use statins is safe during pregnancy true or false:
False
Examples of bile acid-binding resins are:
Cholestipol, colesevelam, cholestyramine
Drug interactions of bile acid-binding resins include
Decreased absorption of certain drugs such as aspirin, digitalis, statins, tetracycline and warfarin
Constipation and bloating
Decreased absorption of fat soluble vitamins
these are the major side effects of what drugs

Bile acid binding resins
What is the MOA of colestipol, cholestyramine, and colesevelam
Increased bile acid excretion in the jejunum and ileum
This increases hepatic conversion of cholesterol to bile acids
The uses of bile acid binding resins include
Type IIa and IIb hyperlipidemias
This antihyperlipidemic drug works by decreasing sterol intestinal absorption
Ezetimibe
Risk of this is increased when taking statins concurrently with ezetimibe
Hepatic dysfunction
Fibrates increase or decrease plasma levels of sterol absorption inhibitors
increase
Clinical uses of ezetimibe are:
primary hypercholesterolemia and phytosterolemia
The side effects of niacin
FIGHT: Flushing, Itching, GI upsets, Hepatic dysfunction, Hyperglycemia and Hyperuricemia, Tachyarrhythmias
The flushing caused by niacin is due to:
Increased prostaglandins (can be alleviated by aspirin)
The MOA of Niacin is
1.Decreased plasma VLDL - decreased hepatic VLDL output by decreased TG synthesis, increased ApoB degradation and decreased FFA from adipocytes by inhibiting hormon sensitive lipase
2.Decreased lipoprotein
3.Increased plasma HDL

5 uses of niacin include:
Hypercholesterolemia (IIa)
Combined hyperlipidemia (IIb)
Dysbetalipoproteinemia (III)
Hypertriglyeridemia (IV)
Lp(a) hyperlipoproteinemia



Gallstones, myositis and elevated liver enzymes are the major side effects of what drug
Fibrates
The two main fibrates are
fenofibrate and gemfibrozil
The main MOA of fibrates is
PPAR-alpha activation
(Peroxisome proliferator activated receptor)
Which types of dyslipidemia are fibrates most useful in treating
III and IV
Fibrates increase LPL expression in these cells causing increased plasma TG hydrolysis
Endothelial cells
The altered enzymatic expression leads to
Increased beta oxidation of FFAs in myocytes
Fibrates cause increased expression of these apoproteins
A-I and II
Fibrates decrease expression of this apoprotein associated with VLDL
ApoC-III
Antiplatelet drugs can be divided into what two categories
Activation and aggregation inhibitors
Major clinical uses of aspirin are:
prophylaxis of MI and stroke
Irreversible inhibition of COX-1 is characteristic of which drug
Aspirin
COX-1 is involved in the conversion of:
Arachidonic acid to Prostaglandin G2
Suppression of platelet activation and aggregation is made possible by this AA derivative
Thromboxane
Salicylism is a dose dependent side effect of aspirin that includes:
Reversible vertigo, vomiting, tinnitus and hearing loss
The side effects of toxic levels of aspirin include:
Respiratory changes (increased respiration, respiratory alkalosis and respiratory depression), Glucose intolerance, Metabolic acidosis and Fever
Irreversible blockade of ADP receptors is the MOA of
Clopidogrel
The ADP receptor is a _______ receptor and therefore blockage of it causes decreased levels of __________.
Gi-coupled; cAMP - this leads to decreased degranulation which suppresses platelet activation and aggregation
Clinical uses of clopidogrel (plavix) are
Prophylaxis of MI and CVA (esp in patients intolerant of aspirin, acute coronary syndrome, and placement of a coronary stent
Major side effects of clopidogrel are:
Bleeding, Irritated GI tract, TTP and Neutropenia
Clopidogrel and ticlopidine are examples of
ADP antagonists
This is a phosphodiesterase inhibitor indicated for intermittent claudication
Cilostazol
Two MOAs of dipyridamole include
Adenosine uptake inhibition
PDE 3 inhibition
Both of which lead to increased intracellular cAMP

This antiplatelet drug is indicated for prophylaxis of thromboemboli in patients with prosthetic heart valves and cardiac perfusion scan
Dipyridamole
The major side effects of dipyridamole are:
Cutaneous rash, Angina elicited by "steeling" of blood in CAD, Disturbed GI tract
The adenosine receptor blocked by dipyridamole is what type of receptor
Gs
This is a glycoprotein IIb/IIIa inhibitor
ABCIXIMAB
The side effects of abciximab are
Bleeding and thrombocytopenia
Clinical uses of Abciximab are
Angioplasty and acute coronary syndrome (unstable angina/Non-Qwave MI)
Alpha granules contained in platelets contain
Fibrinogen, platelet-derived growth factor, platelet activating factor, Factor V and VIII, TGFalpha
Delta granules of platelets contain:
Serotonin, Ca2+, ADP, ATP, Histamine and Epinephrine
This drug is a nonselective and reversible COX inhibitor
Ibuprofen
Clinical uses include
Inflammation (rheumatologic diseases)
Patent ductus arteriosus
Ibuprofen can decrease the effects of this drug
Aspirin
Major side effects of IBUPROFEN
GI Irritation
Bleeding
Ulcers
Pruritis
Rash
Ototoxicity
Fluid retention
Eye disturbances (blurred vision)
Effects of diuretics decreased
Nephrotoxicity
Asthma worsening and Aseptic meningitis









Corticosteroids cause decreased prostaglandins and leukotriene by
Increased lipocortin and decreasing COX-2 expression
Major side effects of inhaled corticosteroids
Hoarseness, Oropharyngeal candidiasis, possible growth suppression in children and eye disorders
Corticosteroids decrease inflammation by decreasing:
Prostaglandin and leukotriene production
Proinflammatory cytokines and chemokines
Vascular permeability and extravasation
Eosinophil, basophil and lymphocyte infiltration


These drugs typically end in -OXETINE
SSRIs
SSRIs interact with what P450 substrate
2D6- causes inhibition
Major side effects of SSRIs include
Sick stomach leading to anorexia, nausea, etc
Sexual dysfunction
Restless: agitation, anxiety and tremor
Insomnia
Sertonin syndrome- Caused by concurrent use of MAOIs



Indications of SSRIs are:
Depression, OCD, Panic disorder, Bulimia nervosa, and social phobia
Diazepam is a
Benzodiazepine
After binding to the GABAa receptor, benzos increase the ________ of channel opening
frequency
Clinical uses of benzodiazepines are (DIASEPAM)
Diagnosis in psychiatry
Insomnia
Anxiety
Skeletal muscle spasticity, status epilepticus
Ethanol or other sedative-hypnotic withdrawal
Procedures needing sedation
Anesthesia
Mania






Drowsiness, confusion and lethargy, dependence and tolerance, Impaired judgment, motor skills and driving ability, Anterograde Amnesia and decreased cognitive function, suppression of respiration and circulation and even death are side effects of:
Benzodiazepines
Binding of GABA causes release of what ion and does what to the membrane
Cl-; hyperpolarization
Flumazenil is a:
Benzodiazepine receptor blocker; decreases recovery time from anesthesia or other medical procedures
-azolam and -azepam are common endings to this class of drugs
Benzos
GABA binds to which subunit of the GABAa receptor
Alpha and beta
The site of binding of benzodiazepines is between which two subunits of the GABAa receptor
Alpha and gamma
Barbiturates lead to hyperpolarization of the cell membrane by having what effect on the GABAa receptor
Prolonging the duration of Cl- channel opening
Clinical indications for barbiturates are:
anxiety, insomnia and seizures, induction of anesthesia
Side effects of barbiturates are:
Dependence and tolerance, P450 induction, Drowsiness, confusion and lethargy, Hangover effects after use as a hypnotic, Porphyrin synthesis induction thus contraindicated in porphyria, higher risk of suppressing the respiratory and CV systems than benzos
Ipratropium works by blocking these receptors
Muscarinic
M3 receptors are this subtype:
Gq meaning they increase IP3/DAG and ultimately Ca2+ levels to cause smooth muscle contraction
Uses of ipratropium bromide are
COPD, acute-relief asthma (used as alternate to/ or synergistically w/ short acting B2 agonists
This drug is an opioid antagonist used after overdose
Naloxone
Clinical indications of opiates
Cough, Heroin/Opioid addiction, Edema (acute pulmonary), Anesthesia, Pain, especially severe and constant, Diarrhea
Opioid stimulates these receptors
Gi-coupled receptors
These opioids are particularly effective at treating cough
Codeine and dextromethorphan
Loperamide and diphenoxylate are opiates that are typically used for
Diarrhea
Morphine is associated with what receptor subunit
Mu
Enkephalin is associated with what opioid receptor subunit
delta
Dynorphin is associated with what opioid receptor subunit
Kappa
Opiates inhibit the release of which neurotransmitters
5-HT, Substance P, ACh, NE and glutamate
Binding of opiates to the opioid receptors causes the opening and closing of which ion channels
Opening of K+ and closing of Ca2+; leads to decreased synaptic transmission
Name the (many) side effects of MORPHINE
Miosis, Orthostatic hypotension, Respiratory depression, Pruritis, High intracranial pressure, Intestinal immobility (constipation), Nephritic suppression (urinary retention), Emesis, Dependence and tolerance, tremor and restlessness
Rank the effectiveness of Ca2+ channel blockers on vascular smooth muscle from most to least
Nifedipine> Ditiazem > Verapamil
Rank the effectiveness of Ca2+ channel blockers on the heart from most to least
Verapamil > Diltiazem > Difedipine
Diltiazem and verapamil slow these phases of the action potential in cells of the SA and AV node
Phase 4 and 0
Cardiac specific Ca2+ channel blockers are indicated for
HTN, Arrhythmias (AVN or AV reentrant paroxysmal supraventricular tachycardia) and angina pectoris
Dihydropridines as a subclass of what
Ca2+ channel blockers
These Ca2+ channel blockers are NOT used for Arrhythmias
Dihydropyridines
Side effects of diltiazem and verapamil
Congestive heart failure, AV block and bradycardia, low blood pressure, Constipation, Increased water retention, Lassitude (Lack of energy)
Treatment of beta blocker intoxication involves
Glucagon, atropine and isoproterenol
Actions of Beta blockers in lowering blood pressure include
Decreasing cardiac output by blocking cardiac beta1 receptors
Decreasing renin release from the kidney by blocking beta1
Decreasing peripheral presynaptic NE release by blocking beta1 receptors



Beta blockers are useful in treating angina pectoris because they
Decrease heart rate and contractility leading to decreased O2 consumption
The action of Beta blockers in treating glaucoma is
Decrease aqueous humor secretion
Beta blockers (esp. propranolol and esmolol) are effective at treating supraventricular tachyarrhythmias because they
Decrease AV conduction velocity
These drugs are mixed alpha1 and beta blockers
Labetalol and carvedilol
Labetalol and carvedilol lead to vasodilation by:
Blocking alpha1 and beta2 activation
Nonselective beta blockers cause what three major effects
cardiac suppression
Nonselective Beta blockers can what three effects
Cardiac suppression
Decreased intraocular pressure
Smooth muscle constriction- due to B2 blockade in airways and blood vessels

Nonselective beta blockers have many more side effects than selective and include:
Airway spasm especially in patients with asthma and COPD
Blood vessel spasm
Masking of hypoglycemia in diabetics
Cardiac suppression and block
Depression, disturbed sleep and impotence
Dyslipidemias
Elevated plasma K+ levels
Fall of blood glucose levels at high doses
Grave withdrawal syndrome







The heparin antidote is
Protamine sulfate
Heparin works by activating what
Antithrombin III
Heparin use prolongs which pathway of the coagulation cascade
Intrinsic pathway, prolonging the activated partial thromboplastin time (aPTT)
Heparin is indicated for the treatment of
PE, DVT, MI, unstable angina, AF, stroke, acute coronary syndrome
By activating AT III, heparin indirectly inhibits clotting factors:
IIa, IXa, Xa, XIa, and XIIa
Thrombocytopenia, Allergy, loss of hair, osteoporosis, increased release of lipoprotein lipase and decreased synthesis of adrenal aldosterone are side effects of
Heparin; in addition to bleeding with a prolonged aPTT of course
3 differences between heparin and LMWHs
LMWHs have 2-4x longer half-lifes, can be administered subcutaneously without laboratory monitoring, act more specifically on factor Xa
In heparin induced thrombocytopenia, IgG autoantibodies form against:
the heparin-platelet factor 4 complex, leading to thromboembolism
This is used as an alternate to heparin for treating patients with HIT
Lepirudin, bivalirudin
Lepirudin and bivalirudin work by
Direct thrombin (IIa)inhibition; recombinant form of hirudin from leeches
Warfarin inhibits this enzyme found in the liver
Vitamin K epoxide reductase
Without the action of vitamin K reductase, this enzyme cannot convert the precursors of factors II, VII, IX and X to their mature forms
Glutamate carboxylase
Which anticoagulant, heparin or warfarin, crosses the placenta
Warfarin
The structure of heparin is a:
Large anionic, acidic polymer
The structure of warfarin is
Small lipid-soluble molecule
The onset of action of warfarin is slow due to
Limitation of half-lives of normal clotting factors
The antidote of warfarin is
Vitamin K1 and fresh frozen plasma

This drug is used in the early phase of thrombotic stroke, acute myocardial infarction and pulmonary embolism
Alteplase (t-PA)
The MOA of alteplase is:
Cleaving plasminogen to form plasmin
Fibrinolytic inhibitors are
Aminocaproic and tranexamic acid
Thrombolytics are contraindicated in patients
With active bleeding, hx of intracranial bleeding, recent surgery, known bleeding diatheses or severe hypertension
This thrombolytic is fibrin/clot specific in action
Alteplase
Streptokinase and urokinase function by
Binding to and activating plasminogen, which then cleaves free plasminogen to form plasmin
In addition to bleeding, streptokinase has what other side effects
Allergic reactions and resistance due to antistreptococcal antibodies
Anistreplase activates both
Streptokinase and plasminogen
Longest known human gene which can lead to increased rate of spontaneous mutation

Dystrophin gene
IN DMD, weakness begins where and progress _____________
Pelvic girdle muscles; superiorly
Increased bulk with decreased strength is
Pseudohypertrophy
Incidence of DMD is roughly
30 in 100,000 births
Diagnosis of muscular dystrophies involves
Elevation in CPK - can be 20-100 times normal
Muscle biopsy- shows muscle destruction, absence of dystrophin, reduction in sarcoglycans and CT and fat in place of muscle
Dystrophin is important in
Anchoring muscle fibers especially in skeletal and cardiac muscle
Although do not develop MD, female carriers can experience some symptoms such as
mild muscle weakness, muscle cramps and elevates creatine kinase levels
Loss of the DAP complex in DMD causes the sarcolemma to be disrupted allowing
unregulated Ca2+ ions to enter, causing necrosis of the muscle fiber
By age 12, patients with DMD are
wheelchair bound
The storage form of vitamin D
25-OH D3
Active form of vitamin D
1,25-(OH)2D3 (calcitriol)
Ergocalciferol is
Vitamin D2 ingested from plants, used as pharmacologic agent
Cholecalciferol
Vitamin D3- consumed from milk, formed in sun-exposed skin
Excess Vitamin D causes
Hypercalcemia, hypercalciuria, loss of appetite, stupor
Deficiency of vitamin D leads to _______ in children , ___________ in adults and __________ in all
Rickets; osteomalacia; hypocalcemic tetany
How does parathyroid hormone (PTH) affect calcium and phosphate reabsorption
Increases Ca2+ but decreases phosphate reabsorption
Decreased levels of both Calcium and phosphate do what to 1,25-(OH)2 production
Increase
25-OH vitamin D is converted to 1,25-(OH)2 Vitamin D by what cells
Proximal tubule cells
This vitamin is found in liver and leafy vegetables
A
Deficiency of vitamin A causes
Night blindness, dry skin
Excess vitamin A can cause
Anthralgias, fatigue, headaches, sore throat, alopecia, dry and pruritic skin, enlarged and cirrhotic liver and a rise in intracranial pressure
Taking isotretinoin during pregnancy can lead to
cleft palate and cardiac abnormalities
Function of Vitamin A includes:
Maintence of vision and reproduction, differentiation of epithelial cells into specialized tissue, and promotion of growth
These are sensitive diagnostic markers for heart failure
Brain natriuretic peptide and pro-BNP
BNP is first synthesized as _____ then cleaved to
Prepro-BNP; pro-BNP
Factors that cause ventricular myocytes to release BNP are
Distention
Sympathetic stimulation
Endothelin
Angiotensin II stimulation


Some of the effects of BNP include
Natriuresis and diuresis
Improved glomerular filtration rate and fraction
Inhibition of renin release
Systemic vasodilation
Arterial hypotension
Reduced PCWP




Recombinant form of human TNF receptor that binds TNF
Etanercept (Enbrel)
Anti-TNF antibody
Infliximab
Directly binds TNF-alpha receptor sites
Adalimumab
Major side effects of TNF-alpha blockers include
Infusion reactions
Infections
Induction of ANAs, double-strantded DNA (dsDNA) and rarely lupus-like syndrome
Increment in lymphomas


Folic acid analog that inhibits dihydrofolate reductase
Methotrexate
Methotrexate works at what phase of the cell cycle
S phase
Inhibition of this enzyme causes decreased dTMP and therefore decreased DNA and protein synthesis
Dihydrofolate reductase
Non-neoplastic uses for methotrexate include
Ectopic pregnancy, Abortion, RA, psoriasis
This is used to rescue normal cells in the bone marrow from toxic effects of methotrexate
Leucovorin (Folinic acid)
Nephrotoxicity, neurotoxicity, interstitial pneumonitis, hepatotoxicity, alopecia, disturbed GI tract and bone marrow suppression are side effects of
Methotrexate
Bamboo spine on x-ray
Ankylosing spondylitis
Systemic inflammation, joint pannus, boutonniere deformity =
Rheumatoid arthritis
HLA-DR3 or DR4
DM, RA, SLE
Classic presentation of RA includes
Morning stiffness lasting >30 min and improving with use, symmetric joint involvement, systemic symptoms (fever, fatigue, pleuritis, pericarditis)
Affects females> males, type III hypersensitivity, strong association with HLA-DR4
RA
Characteristics of RA
Autoimmune
Fibrinoid necrosis surrounded by palisading histiocytes
Subcutaneous rheumatoid nodules
occurs in approximately 10% of patients with psoriasis
Psoriatic arthritis
An immunoglobulin (most often IgM) with anti-IgG Fc specificity
Rheumatoid factor
Most common cause of dementia
Alzheimer disease
Amyloid deposit in and about vessels
Amyloid angiopathy
Intracytoplasmic proximal dendritic eosinophilic inclusions consisting of actin
Hirano bodies
Intracytoplasmic bundles of filaments derived in part from microtubules and neurofilaments, occur within neurons especially in the cerebral cortex
Neurofibrillary tangles
Aggregates of these form the amyloid of neuritic plaques and nearby cerebral vessels
A(beta)40 amyloidogenic peptide
This gene found on chromosome 21 encodes for amyloid precursor protein
APP gene
Alzheimer like abnormalities occur in:
Trisomy 21 (Down syndrome)
This allele occurs with greater frequency in patients with Alzheimer disease
Eta4 allele of apoprotein E (chromosome 19)
Swollen nerve cell processes occuring in spherical focal collections in the cerebral cortex, hippocampus, and amygdala
Neuritic (senile) plaques
Generalized cerebral atrophy in Alzheimers is most prominent in which areas:
Frontal and hippocampal, sulci are widened because of narrowing of gyri
Morphologic characteristics of ALS
Degeneration and atrophy of the lateral corticospinal tracts and anterior motor neurons of the spinal cord
Degeneration of upper and lower motor neurons is characteristic
Amyotrophic lateral sclerosis
Clinical manifestions of ALS include
Symmetric atrophy and fasciculation (LMN signs) and hyperreflexia, spasticity and pathologic reflexes (UMN signs)
Onset of ALS typically occurs
In early middle age; death from respiratory failure occurs in 1-6 years
Protein aggregates in neurons from hyperphosphorylation of protein tau
Neurofibrillary tangles (First Aid)
These cells are destroyed in MS
oligodendrocytes
Can be caused by a defect in superoxide dismutase
ALS
This neurotransmitter is decreased in MS
ACh
Incidence of MS is directly proportional to
geographic distance from the equator
More common in women and presents most often between 20 and 30 years of age
Multiple sclerosis
Possible lab findings in MS include:
Increased protein IgG in CSF
MRI is gold standard
Periventricular plaques with preservation of axons

Treatment for MS involves
Interferon beta or immunosuppressants
Symptomatic treatment for neurogenic bladder, spasticity, pain
Patients with MS can present with
Optic neuritis (sudden loss of vision), MLF syndrome (internuclear ophthalmoplegia), hemiparesis, hemisensory symptoms or bladder/bowel incontinence
This may be a protective factor to the development of multiple sclerosis
Sun exposure; increased prevalence rates at higher latitudes and vitamin D deficiency is associated with increased risk
This drug has a black box warning due to the severe hematologic adverse reactions associated with its use
Ticlopidine

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