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MedChem533 ExamIII
| Question | Answer |
|---|---|
| ___ ___ ___ is the peak pressure at time of contraction of the heart. | systolic blood pressure |
| ___ ___ ___ is the minimum pressure is at the time of relaxation. | diastolic blood pressure |
| For the heart to pump in an efficient manner there must be a ___ contraction of the individual muscle fibers. | contraction |
| The heart muscle consists of a variety of ___ (nodal, conducting, and general). | myocytes |
| Since the atria must contract before the ventricle, the initiating impulse from the ___ ___ travels of over the atria and is prevented from reaching the ventricle by a layer of non conducting tissue. | sinoatrial node |
| This non conducting tissue separates the atria and ventricle except at one point called the ___-___ node. | atrio-ventricular |
| On emerging from the AV node, the signal is picked up by the tissue known as the ___ __ ___ which passes it to the even faster conducting myocytes known as the ___ ___. | Bundle of His, Purkinje fibers |
| There are three electrical events in the heart: ___ of the signal, ___ of the signal, and ___ of the signal. | generation, conduction, dying |
| Muscles contract because of an interaction between the protein ___ and ___ which causes a physical shortening of the cell. | actin, myosin |
| Typically actin and myosin are prevented from interacting by the protein ___ but exposure to elevated ___ levels overcomes this regulation. | tropomyosin, calcium |
| In cardiac muscle, an influx of calcium ions via ___ of the cell and associated internal release of calcium stores causes contraction. | depolarization |
| ___ ___: sustained elevated pressure of unknown cause. | essential hypertension |
| ___ ___: sustained elevated pressure of known cause. | secondary hypertension |
| ___ complication of hypertension are thought to be due to the raised arterial pressure and associated ___ of major arterial circuits. | atherosclerosis |
| In the brain, ___ ___ leads to increased vascular resistance via interaction with V1 and vasodilation by activating V2 receptors. | arginine vasopressin |
| In the sympathetic nerves, ___ release leads to increased resistance. | norepinephrine |
| In the blood vessels, ___ release leads to hypertrophy and constriction. | endothelin |
| In the blood vessels, ___ ___ is synthesized from arginine and its release stimulates cGMP production and smooth muscle relaxation. | Nitric oxide |
| In the kidneys, ___ release and generation of ___ ___ leads to vasoconstriction. | renin, angiotensin II |
| In the heart, release of the ___ ___ ___ causes vasodilation via interaction with vascular receptors. | atrial natriuretic factor |
| ANF also has ___ properties. | diuretic |
| Arterial blood pressure is directly proportional to the product of ___ ___ and the ___ ___ ___. | cardiac output, peripheral vascular resistance |
| In individuals cardiac output and peripheral resistance are controlled by two overlapping mechanisms: ___ mediated by the sympathetic nervous system and ___ ___ system. | baroreflexes, renin angiotensin |
| Most antihypertensives either ___ cardiac output or ___ peripheral resistance. | reduce, decrease |
| ___ involving the sympathetic nervous system are responsible for the rapid regulation of blood pressure. | Baroreflexes |
| A fall in blood pressure causes pressure sensitive neurons (baroreceptors) to send ___ impulses to the cardiovascular centers in the ___ ___. | fewer, spinal cord |
| Long term control of blood pressure is mediated by the ___ and the ___. | RAS, kidney |
| The kidnes respond to baroreceptors by releasing ___. | renin |
| ___ ___ is the body's most potent circulating vasoconstrictor. | Angiotensin II |
| In the treatment of hypertension three approaches are considered: reduce ___ overload, reduce ___ outflow from the brain, ___ blood vessels. | volume, sympathetic, dilate |
| ___-___ and ___ are front line therapy in treatment of hypertension. | beta-blockers, diuretics |
| ___: reduce blood pressure and edema by increasing urine production. | diuretics |
| ___: inhibit release of adrenergic agonists or antagonizing adrenergic receptors. | antiadrenergics |
| ___: suppress synthesis of angiotensin II, prevent calcium influx. | vasodilators |
| The overall action of ___ is to increase the reabsorption of sodium and secretion of potassium. | aldosterone |
| ___ ___ act on the kidney to increase urine flow, decrease electolyte reabsorption by the tutubles and maintain osmotic balance, increase water excretion, decrease blood volume, and decrease cardiac output. | thiazide diuretics |
| Beta-___ blockers reduce heart rate, reduce cardiac output, decrease renin secretion, reduce angiotensin II, and decrease peripheral resistance. | adrenoreceptor |
| alpha adrenergic receptor antagonists block the action of ___ and ___. | catecholamines, epinephrine |
| Catecholamines and epinephrine would caue ___. | hyperteinson |
| blockade of catecholamines and epinephrine receptors reduces ___ ___ of the blood vessels, resulting in decreased peripheral vascular resistance, and lower arterial blood pressure by causing the relaxation of both arterial and venous smooth muscle. | sympathetic tone |
| Nitrates, hydralazine, minoxidil, and diazoxide are direct acting ___. | vasodilators |
| ___ acting vasodilators act at smooth muscle cells to reduce the excitability of the vasculature to a variety of stimuli by influencing cellular contraction mechanisms. | direct |
| ___ vasodilators produce their effect by interfering with the vasocnstrictor and thus their primary site of action is not necessarily smooth muscle. | indirect |
| alpha-adrenoreceptor antagonists, ACE, and angiotensin II are ___ vasodilators. | indirect |
| hydralazine effects intracellular ___ levels. | calcium |
| Sodium nitroprusside releases ___ ___. | nitric oxide |
| Minoxidil/Pinacidil/Diazoxide appear to produce vasodilation by activation of the ATP dependent ___ channels. | potassium |
| ___ relax smooth muscle tissue, resulting in diminished venous return to the left ventricle, and thus the heart is unable to expel the blood being delivered to it. | nitrites |
| Nitrites are anti-___ agents. | ichemic |
| Nitrites have two mechanisms: vasodilation of the ___ system and vasodilation of the ___ ___ ___. | venous, large coronary arteries |
| ___ ___ ___ inhibiti excitation-contraction coupling, resulting in vasodilation and fall in blood pressure. | calcium channel blockers |
| An important focus of calcium antagonists has been myocardial ___. | protection |
| All calcium channel antagonists share the common feature of competitively blocking the cell membrane ___ channels, resulting in decreased calcium influx into the cell during the ___ state. | slow, active |
| Calcium antagonists block the ___-___ channels in vascular tissue resulting in relaxation of smooth muscle and in cardiac tissue, resulting in a negative ionotropic effect. | L-type |
| Generation of the signal for heart muscle contraction depends on the ___ ___. | sinoatrial node |
| conduction of the signal for heart muscle contraction depends on the ___ __ ___ and ___ ___ of the ventricle. | bundle of His, Purkinje fibers |
| The depolarization of the cell allows catalytic quantities of ___ to enter the cell which cause a large release of calcium ions from the ___ ___. | calcium, sarcoplasmic reticulum |
| The ___-___ law states the force of contraction is proportional to fiber contraction. | Frank-Starling |
| In the absence of depolarization, the Ca/ATPase pumps on the SR remove intracellular calcium ions to restore the ___ state of the cell. | resting |
| ___: increase in blood pressure by a greater force of contraction. | inotropism |
| ___: blood pressure is increased by an increase in frequency of contraction. | chronotropism |
| ___: increase urine production. | diuretics |
| ___: inhibit release of adrenergic agonists or antagonize adrenergic receptors. | antiadrenergics |
| ___ ___: act on smooth muscle and influence cellular contraction mechanism. | direct vasodilators |
| ___ ___: effect vasoconstrictors | indirect vasodilators |
| Angiotensinogen is cleaved by the protease ___ to form angiotensin I. | renin |
| Angiotensin I is acted upon by ___ ___ ___, a zinc metalloprotease that hydrolyzes carboxyterminal dipeptides, to form Angiotensin II | angiotensin converting enzyme |
| Angiotensin II is converted to Angiotensin II by ___ ___, that selectively cleaves the aspartyl residue. | aminopeptidase A |
| The amino terminal arginine residue of AngIII is cleaved by ___ __ to form AngIV | aminopeptidase M |
| AngI can be directly converted to AngIII by ___. | ACE |
| Renin is synthesized (from preproprotein) and stored in the ___ cells of the afferent arteriole in the ___. | juxtaglomerular, kidney |
| One of the actions of ACE that may influence blood pressure is the conversion of ___ to ___ and inactivation of the vasodepressor nonapeptide ___. | AngI, AngII, bradykinin |
| ___: a vasodepressor at local tissue level especially of capillaries. | bradykinin |
| Binding of ___ ___ to its receptors results in the stimulation of phospholipase C, increasing intracellular inositol triphosphate levels and intracellular diacylglycerol. | Angiotensin II |
| cAMP is produced when a G protein activates ___ ___. | adenylate cyclase |
| Activation of phospholipase C hydrolyses PIP2 to produce ___ and ___ ___. | diacylglycerol, inositol triphosphate |
| DAG activates ___ ___ ___ whereas IP3 releases ___ from intracellular stores. | protein kinase C, calcium |
| Inhibitors of ___ ___ exert their effect by inhibiting the proteolysis of ANF, and endogenous peptide with vasodilatory and diruetic properties. | neutral endopeptidase |
| Inhibitors of renin, angiotensin converting enzyme, and angiotensin II are effective antihypertensive agents that ultimately prevent the increase in intracellular ___ ions and the resultant ___ of vascular smooth muscle. | calcium, constriction |
| ___ resulted from an appreciation of how angiotensinogen bound to renin and centered upon transition state analogs. | Enalkiren |
| ___ was discovered by proposing an active site model, with consideration of the physiological substrate, and then optimizing substitutents to interact with the active site Zn cation, hydrogen bonding and positive charge sites. | Captopril |
| ___ originated from an imidazole screening lead which was optimized by mimicking the conformational and functionality of angiotensin II. | Losartan |
| Class __ antiarrhythmics are local anesthetics that slow conduction in nerve and myocardial cell membranes. | 1 |
| Class 1___ antiarrhythmics decrease maximal rate of depolarization while increasing duration of mycardial action potential. | A |
| Clas 1___ antiarrhythmics decrease maximal rate of depolarization while decreasing duration of myocardial action potential. | B |
| Class 1___ antiarrhythmics decrease maximal rate of depolarization while having no effect on duration of myocardial action potential. | C |
| Class ___ antiarrhythmics are beta-adrenergic blockers that block the adrenergic neurons. | II |
| Class ___ antiarrhythmics cause homogeneous prolongation of the duration of the myocardial action potential. | III |
| Class ___ antiarrhythmics are calcium channel blockers. They block the slow inward current of the Ca ions during myocardial action potential. | IV |
| ___: an unwanted clot inside a blood vessel. | thrombus |
| The ___ ___ ___ is that early and full reperfusion should be the goal of acute revascularization strategies. | open artery hypothesis |
| ___ are administered to destroy clots that have already formed. | fibrinolytics |
| The molecular targets for preventing coagulation/clot formation are ___, ___, and/or ___. | thrombin, Xa, VIIa |
| Molecular targets of platelet aggregation inhibition are ___, and the ___ receptor. | P-selectin, thrombin |
| ___ drugs are used extensively in myocardial infarction to lyse thrombi that block coronary arteries. | fibrinolytic |
| ___ catalyzes the conversion of soluble fibrinogen into fibrin monomers I and II, and activates factor XIII to XIIIa to cross link into a stable insoluble clot. | Thrombin |
| ___ is a glycosaminoglycan composed of a mixture of polysaccharides which on its own has little anticoagulant effect, but upon association with ATIII this effect is increased. | heparin |
| ___ is a naturally occuring protein mainly found along the endothelial lining and is part of an endogenous mechanism regulating thrombin formation. | ATIII |
| ___ are anucleate cell fragments shed by megakaryocytes in the bone marrow that are involved in the genesis and expression of coronary artery heart disease. | platelets |
| ___ and ___ appear to be primarily responsible for platelet activation | Collagen, IIa |
| ___ is a member of the integrin family of adhesion molecules and ultimately links adjacent platelets together thereby forming aggregates. | GPIIb/IIIa |
| ___ ___: an inherited deficiency of GPIIb-IIIa characterized by platelets that do not bind adhesive proteins and therefore fail to aggregate, resulting in the life long bleeding diathesis. | Glanzmann's thrombasthenia |
| ___ are a family of alphabeta heterodimers that mediate adhesion of cells to extracellular matrix proteins and to other cells. | Integrins |
| ___ refers to neovascularization of new blood vessels from pre-existing ones. | neovascularization |
| Cardiovascular disease is a result of coronary artery disease leading to ___ ___. | myocardial infarction |
| Cardiovascular disease is a result of cerebrovascular disease leading to ___. | stroke |
| Cardiovascular disease is a result of venous thrombosis predisposing to ___ ___. | pulmonary embolism |
| ___: deposition of lipids and extracellular matrix resulting in the formation of plaques in the intima of the large and medium-sized arteries, often associated with a reduction in the arterial lumen and a predisposition to thrombosis. | Atherosclerosis |
| Secondary manifestations of ___ include angina pectoris, myocarial infarction, stroke, periphery artery diseease. | Atherosclerosis |
| ___: having the capacity to initiate or accelerate the process of atherosclerosis. | atherogenic |
| ___: fatty substances circulating in the blood stream including cholesterol, cholesteryl esters and triglycerides. | lipids |
| ___: abnormally increased plasma cholesterol. | hypercholesterolemia |
| ___: abnormally increased plasma triglycerides. | hypertriglyceridemia |
| ___: abnormally increased levels of plasma lipids. | hyperlipidemia |
| ___: miscelle composed of lipid and protein utilized by the body to transport cholesterol, cholesteryl esters, and triglycerides. | lipoprotein |
| ___: protein moiety associated with lipoprotein, so-called navigator of lipoprotein, often serve as ligands for receptors involved in processing of lipoproteins. | apolipoprotein |
| ___: an insoluble lipid which gives rigidity to membranes and serves as the precursor to hormones. | cholesterol |
| Plasma lipoproteins are spherical particles which are composed of ___ with fatty acids arranged in the center of the particle. | phospholipids |
| Cholesterole is particularly important to the ___ which is rich in it. | CNS |
| ___ do not produce cholesterol but instead sitoserol which is present in 100-200mg/day. | plants |
| Chylomicrons transport cholesterol from the ___ to the ___. | intestine, liver |
| Chylomicrons have a non-polar core consisting primarily of ___. | triglycerides |
| Brown and Goldstein discovered that the underlying mechanism to the severe hereditary familial hypercholesterolemia is a complete, or partial, lack of functional ___-___. | LDL-receptors |
| Oxidation of ___ in LDL via malonaldehyde or reactive oxygen species results in oxidized LDL. | apoB |
| Oxidized LDL is recruited and trapped in the intima of the vessel wall where they are absorbed into macrophages to become ___ cells and is the first step in ___. | foam, atherosclerosis |
| ___ ___ ___ is the process whereby HDL continuously picks up cholesterol from cells, esterifies it, and facilitates its transfer to other lipoproteins and elimination. | reverse cholesterol transport |
| In the early stages of liver disease there is a hepatic ___ deficiency which leads to elevated HDL. | lipase |
| In the end stage of liver disease LCAT deficiency leads to HDL ___. | deficiency |
| ___ lesion: potentially unstable, little or no angiographic abnormality, more lipid rich, immature. | non-occulsive |
| ___ lesion: often stable, abnormal angiogroen, more fibrous, mature. | stenotic |
| Niacin in cholesterol lowering doses causes ___ ___ by stimulating biosynthesis of prostaglandin D2, especially in the skin. | facial flushing |
| PG D2 acts as a vasodilator via DP1 receptors increasing blood flow and thus leading to ___. | flushes |
| ___ reduces facial flushes induced by niacin. | Laropiprant |
| ___ ___ protein facilitates the movement of cholesterol ester from HDL to LDL in exchange for triglycerides. | cholesterol transfer |
| Statins in both LDL dependent and independent pathways elevate ___ ___ leading to small blood pressure ___. | nitric oxide, lowering |
| Statins also work by depleting ___, preventing pro-inflammatory proteins. | isoprenoid |
| PCSK9 is an enzyme whose only known substrate is ___. | itself |
| Inflammation is the body's defense against ___ infection. | microbial |
| ___ immunity is generally the same as inflammation, involves a rapid response, is non-specific, and involves mast cells, neutrophils, macrophages, and cytokines. | innate |
| ___ immunity involves a delayed response, is more specific to the particular microbe, and involves T cells, B cells, and antibodies. | adaptive |
| ___ arthritis: a systemic, inflammatory polyarthritis that leads to joint destruction, deformity, and loss of function. | rheumatoid |
| The pathology of RA involves the ___ membranes and ___ structures of multiple joints. | synovial, periarticular |
| Sharp scores take into account ___ scores, ___ ___ ___ scores, and ___ sharp score. | erosion, joint space narrowing, total |
| NSAID= ___ ___ ___ | nonsteroidal antiinflammatory drug |
| DMARD: ___ ___ ___ ___ | disease modifying antirheumatic drug |
| BRM's: ___ ___ ___ | biologic response modifiers |
| ___ have anti-inflammatory and immunoregulatory activity, but nominal disease-modifying capability. | corticosteroids |
| cyclooxygenase inhibitors, aspirin, ibuprofen, naproxen, celebrex, and bextra are all ___. | NSAID's |
| methotrexate and sulfasalazine are both ___. | DMARD's |
| remicade and kineret are both ___. | BRM's |
| Cortisone, dexamethasone, prednisone, and bethamethasone are all ___. | corticosteroids |
| Methotrexate was originally developed as an ___ drug. | anticancer |
| Methotrexate is an inhibitor of ___ ___. | dihydrofolate reductase |
| Methotrexate inhibits ___ and ___ biosynthesis. | purine, pyrimidine |
| Azathiaprene was originally used as an ___ agent. | antiproliferative |
| Azathioprene acts as an ___. | antimetabolite |
| Chloroquine was originally developed as an ___ drug. | antimalarial |
| Leflunomide is a ___ which targets ___ ___. | DMARD, dihydroorotate dehydrogenase |
| Leflunomide causes cell-arrest in ___. | lymphocytes |
| ___ are small proteins similar to hormones and growth factors which regulate the immune system and other cellular responses. | cytokines |
| ___ is necessary for granuloma homeostasis in tuberculosis. | TNF |
| Osteoarthritis is largely a disease of the ___ cartilage. | articular |
| ___: a condition where the tissue contains an excess of body fluids. | edema |
| ___: a medicine that reduces pain | analgesic |
| ___: agents that reduces fever | anipyretic |
| PG ___ ___ converts aracadonic acid to PGH2. | endoperoxide synthase |
| Two distinct PG endoperoxide synthases exist in mammals: COX-1 ___ enzyme and COX-2 ___ enzyme. | constitutive, inducible |
| NSAIDS inhibit ___ activity not ___ activity. | COX, PER |
| A sole amino acid at the inhibitor binding site allows access to a channel in ___ which is blocked in ___. | COX2, COX1 |
| Prostacyclin is a ___, inhibits platelet aggregation and adhesion. | vasodilator |
| Thromboxane A2 is pro-thrombotic, a potent ___, promotes platelet aggregation. | vasoconstrictor |
| ___ kinase is a lipid kinase that phosphorylates PIP2 to PIP3. | Pi3 |
| Thrombin and factor VIIa complement ___ proteases. | serine |
| Interleukin1beta converting enzyme, caspases, and papin are ___ proteases. | cysteine |
| Aspartic proteases contain 2 aspartic acids plus an ordered ___ at their active site. | water |
| HIV protease and renin are ___ proteases. | aspartic |
| Metalloproteases have an active site ___ and glutamic acid. | zinc |
| Stromolysin, collagenase, and angiotensin converting enzyme are all ___. | metalloproteases |
| ___ converts inactive Pro-IL-1beta to active IL-1beta. | ICE |
| ICE is first of a family of proteases known as ___ which are critical for apoptosis. | caspases |
| Metalloproteinases degrade all components of the ___ ___. | extracellular matrix |
| COX2 and COX1 expression in the kidney, endothelial cells, and platelets determine the balance between ___ and ___. | prostacyclin, thromboxane |
| ___ ___ ___ disease: chronic airway disorders that are characterized by airflow limitation that is not fully reversible. | Chronic Obstructive Pulmonary |
| ROS= ___ ___ and ___ ___ | reactive oxygen, nitrogen species |
| ROS-linked modulation involves protein regulation through ___ modifications of cysteine residues from reversible to irreversible forms. | redox |
| In ROS-linked modulation, the ___ of the cysteine residues influences the selectivity and degree of oxidative modification. | environment |
| Activation of Nrf2 is counter-regulatory to ___ and is fundamental for protecting host tissues from oxidative/electrophilic damage. | NF-kB |
| ___ is a transcription factor which when coupled with Maf proteins activates the ARE, suppresses inflammatory pathways, and uses Keap1 to act as a sensor of cellular oxidative stress. | Nrf2 |
| Poly-unsaturated fatty acids convert spontaneously to anti-inflammatory ___. | cyclopentanones |
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