THE PRACTICE TEST
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increased insulin sensitivity in target tissues inhibit or delay the breakdown of carbohydrates in the intestine direct action on the beta cell membrane-bound receptors direct stimulation of insulin receptors in skeletal muscle
rapidly responds to a stimulus is a neurotransmitter binds to specific receptors to produce its effects produces nerve impulses
travel along axons to the posterior pituitary affect the secretion of hormones in the anterior pituitary are released by the target organ to regulate hypothalamus produce nerve impulses
the hypothalamus the posterior pituitary the fat-soluble releasing hormones TSH
elevated thyroid hormone production decreased adrenocorticotropic hormone (ACTH) decreased growth hormone high plasma glucose concentration
CNS anterior pituitary hypothalamus target organ (thyroid gland)
conduct electrical impulses regulate growth control metabolism help in reproduction
it controls the master gland it is composed of two main lobes it is connected by a portal system to the posterior pituitary gland it releases luteinizing hormone
TSH ACTH LH, FSH GH
binding receptors on the cell membranes crossing the plasma membrane being second messengers stimulating gene transcription
levels of circulating hormone always change suddenly and severely the target organ turns off pituitary secretion a baby suckling is an example of negative feedback hormones are NOT controlled by this process
they are secreted by the adrenal medulla the target organ is the pancreas they cause excess excretion of sodium ions their principle action is to reduce inflammation
Addison's disease (generate too little...) Cushing's disease (too much...) thyroid disease rheumatoid arthritis
dehydration hypotension bronchial asthma weight loss
regulate the metabolism of carbohydrates make new protein retention of sodium transcription of nucleus DNA
cause an increase in reabsorption of sodium cause K ion transport to urine regulate fluid balance decrease inflammation
obesity thinning of skin glaucoma increased muscle strength
testosterone estrogen GnRH DHEA
progesterone FSH hCG LH
inhibiting the corpus luteum's production of progesterone facilitating implantation to occur increasing the levels of estrogen and progesterone stimulating the release of LH and FSH
inhibition of phosphodiesterase 5 inhibition of GnRH vasoconstriction of the blood vessels in the penis stimulation of the release of testosterone
the hormone is delivered via a vaginal ring they can be monophasic, biphasic, or triphasic they can be administered as a spray the doses of estrogen are at the highest effective coverage dose
pill color varies over the cycle estrogen to progestin ratio changes over the cycle the first 10 pills of the cycle may be iron supplements there is a fixed ratio of hormones for days 0 to 21
insulin thyroxine cortisol oxytocin
stimulates uterine muscle contraction increases urine output inhibits preterm labor decreases urine output
it increases urine output it regulates water balance the adrenal glands are its target organ its secretion is controlled by ADH-releasing factor
oxytocin and ADH are both polypeptides ADH is the only hormone secreted from the posterior pituitary the release of ADH and oxytocin is caused by another hormone ADH and oxytocin are secreted by the anterior pituitary gland
control of postpartum bleeding decreasing contractions inducing therapeutic abortions uterine tetany
is classified as a mast cell release inhibitor is one of the substances released during an allergic response is found in white blood cells known as neutrophils does not cause skin reactions
are only found in the bloodstream are coated with immunoglobulins that recognize antigens have no other role than antiallergy in the body degranulate when the H 1 -receptor is stimulated
can be blocked only by histamine cannot be prophylactically treated is characterized by itching, sneezing, and edema is only characterized by wheals and urticaria
are the newest, third-generation drugs are effective and can cause drowsiness are not found in OTC products do not have anticholinergic properties
are more selective for peripheral H 1 -receptors bind the H 1 -receptors in the brain to produce fewer side effects are more sedating and drying than diphenhydramine are mast cell stabilizers
promethazine is the only antihistamine with a cautionary (black box) warning antihistamines reduce itching and pain at the sensory nerve endings histamine causes relaxation of bronchiolar smooth muscle hypersensitivity can develop to antihistamines
histamine after it is released H 1 -receptors from binding histamine the release of histamine and other active substances from mast cells the effect of histamine after it binds
promethazine cetirizine loratadine levocetirizine
epinephrine (Adrenaline) ipratropium (Atrovent) salmeterol (Serevent) theophylline (Elixophylline)
fluticasone cromolyn albuterol montelukast
anticholinergics beta adrenergics methylxanthines corticosteroids
produce bronchodilation increase expectoration of mucus inhibit release of mast cell mediators liquefy bronchial secretions
bronchodilation increased mucociliary activity bronchodilation and increased mucociliary activity none of them
cromolyn omalizumab ipratropium guaifenesin
prostaglandins ECF-A leukotrienes only prostaglandins and leukotrienes
bronchodilation increased cyclic AMP increased mucus secretion stimulation of the beta-2 receptors
inhibit release of mediators from mast cells block beta-2 receptors relax smooth muscle only inhibit release of mediators from mast cells and relax smooth muscle
decrease activation of arachidonic acid decrease the expression of pro-inflammatory mediators and pro-allergic antibodies increase the production of pro-allergic antibodies only decrease activation of arachidonic acid and decrease the production of allergic antibodies
cephalic colonic gastric intestinal
alcohol GERD (gastroesophageal reflux disease) NSAIDs (nonsteroidal anti-inflammatory drugs) Helicobacter pylori
antacids H2 -receptor antagonists proton pump inhibitors sucralfate
not enough mucosal lining in the stomach suppressed acid production regurgitation of bile acids into the esophagus hypersecretion of mucus in the stomach
increase mucosal production suppress acid production and relieve symptoms prevent erosion of ileum maintain levels of magnesium and calcium with antacids
prevent labyrinthine stimulation of emesis prevent serotonin from stimulating the CTZ block stimulation of dopamine receptors increase secretions from ECL cells
rifaximin (antibiotic) bulk laxatives lubiprostone (a ClC 2 chloride channel activator) methylnaltrexone
antibiotics opioid derivatives anticholinergics adsorbents
emollients lubiprostone stimulants methylnaltrexone
docusate sodium (laxative to treat constipation in children) polyethylene glycol psyllium hydrophilic (dietary fiber to relieve symptoms of both constipation and mild diarrhea) mineral oil
increased intestinal motility inflammation osmotic imbalance drug therapy
kill bacteria decrease serotonin release form a complex with irritating substance absorbed into blood circulation to work on the system
5-HT 3 antagonists adsorbents antimotility drugs cathartics
soak up water and distend the rectum irritate the mucosal lining of the intestine inhibit stool formation in the large intestine coat the fecal matter
sitagliptin acarbose nateglinide tolbutamide
metformin glipizide sitagliptin miglitol
insulin glucagon humulin GnRH
increased insulin sensitivity in target tissues inhibit or delay the breakdown of carbohydrates in the intestine direct action on the beta cell membrane-bound receptors direct stimulation of insulin receptors in skeletal muscle
insulin is secreted by the beta cells and insulin resistance is present insulin cannot be used in type 2 DM patients are only prone to persistent infections in type 1 DM oral antidiabetic drugs cannot be combined to achieve glycemic control
excess glucose spills into the urine and osmotically attracts water into the renal tubule antidiuretic hormone is no longer secreted in DM GLUT2 receptors move glucose from the blood into the renal tubule sulfonylurea drugs interact with their receptors in the kidney to increase urine flow
insulin secretion? regular human insulin and insulin glargine DPP-4 inhibitor, sitagliptin and metformin amylin and glucagon
insulin and amylin glucagon incretins acetate
lipodystropy is exacerbated by alpha glucosidase inhibitors miglitol and acarbose insulin is the preferred treatment in type 2 DM because there are no drug interactions oral antidiabetic drugs include pramlintide hypoglycemia is the most common adverse effect of many antidiabetic drugs
pancreatitis when cholesterol is 80 to 100 mg/dL plaque when HMG-CoA reductase is 80 to 100 mg/dL plaque when LDL cholesterol exceeds 160 mg/dL arthritis and edema
ezetimibe (Zetia) acts in the intestinal lumen to bind and trap cholesterol fibric acid derivatives act at the brush border of the intestine wall nicotinamide inhibit lipoprotein lipase to lower triglycerides lovastatin (Mevacor) inhibits an enzyme in the cholesterol synthetic pathway
gemfibrozil (Lopid) nicotinic acid (Niacor) atorvastatin (Lipitor) colesevelam (Welchol)
LDL pulls cholesterol out of plaque and returns it to the liver VLDL transports triglycerides apolipoproteins B and E contain a cholesterol core to form LDL and HDL, respectively foam cells are cholesterol-rich macrophages
statins thiazides nicotinic acid fibric acid derivatives
blocking the intestinal absorption of cholesterol inhibiting triglyceride lipase inhibiting the production of mevalonic acid decreasing hepatic VLDL-triglyceride synthesis
reducing LDL and CRP levels reducing HDL levels reducing hepatic CYP3A4 levels reducing acetyl CoA levels
sublingual nitroglycerin tablets nitroglycerin ointment transdermal nitroglycerin IV nitroglycerin (bolus injection)
reduced force of myocardial contraction decreased oxygen consumption decreased cardiac work all of these
decreased AV conduction increased myocardial contraction decreased heart rate only decreased AV conduction and decreased heart rate
nitroglycerin metoprolol nifedipine verapamil
propranolol verapamil nifedipine isosorbide dinitrate
increasing the venous return to the heart reducing atherosclerosis in the arteries increasing cardiac work relaxation of systemic veins and arteries
decreasing cardiac work decreasing force of contractions decreasing oxygen consumption all of these
calcium channel blockers beta-blockers nitrates only calcium channel blockers and nitrates
hyperuricemia (excess of uric acid in the blood) hyperkalemia hypernatremia hypercalcemia
can cause hyperuricemia can cause hyperglycemia can be used to reduce ascites due to malignancy can cause metabolic acidosis
the proximal tubule the loop of Henle the distal convoluted tubule (DCT) the capsule area of glomerular filtration
water potassium glucose acid
anuria is a state where no urine is formed the major tubular secretory function of the nephron involves hydrogen and potassium ions uremia is an accumulation of nitrogen waste products tubular reabsorption of water is diuresis
produce a mild diuresis without acid/base disturbance inhibit aldosterone receptors produce hypokalemia produce similar adverse effects to thiazide diuretics
movement of small molecules into the glomerulus nephron production of calcium carbonate transport of ions into the blood movement of sodium ions into circulation
glomerulus proximal convoluted tubule and collecting ducts distal convoluted tubule uremic channel
tubular secretion of hydrogen ions increasing the pH of the urine neutralizing cell waste products decreasing the production of bicarbonate ions
decrease in release of renin decrease in cardiac output only decrease in heart rate and decrease in cardiac output all of these
reduction of blood volume blockade of alpha adrenergic receptors relaxation of vascular smooth muscle only reduction of blood volume and relaxation of vascular smooth muscle
alpha-blockers beta-blockers angiotensin-converting enzyme (ACE) inhibitors angiotensin receptor blockers
verapamil propranolol prazosin captopril
vasodilation water excretion decreased blood pressure activation of angiotensin I
decreasing peripheral resistance increasing cardiac output increasing excretion of sodium decreasing peripheral resistance and increasing excretion of sodium
decreasing sympathetic nerve activity stimulating inhibitory alpha-2 receptors decreasing release of renin decreasing sympathetic nerve activity and decreasing release of renin
coronary artery disease CHF supraventricular arrhythmias coronary artery disease and supraventricular arrhythmias
Na ions move out of the cell K ions move out of the cell Na ions move into the cell Ca ions move into the cell
IA IB IC II
lidocaine adenosine propranolol amiodarone
decreased heart rate decreased force of myocardial contraction slowed AV conduction vasodilation
Cl Ca Na K
mildly decrease in Phase 0 depolarization prolongation of ventricular repolarization decrease in AV conduction increase in PR interval
premature atrial contractions premature ventricular contractions paroxysmal atrial tachycardia premature atrial contractions and paroxysmal atrial tachycardia
decrease heart rate increase AV conduction decrease automaticity of ventricular muscle decrease heart rate and decrease automaticity of ventricular muscle
arterial dilation elimination of sodium venous dilation increased bradykinin (a peptide cause blood vessel to dilate)
block aldosterone receptors increase sodium excretion at loop of Henle block sodium channels (ENaC) at nephron collecting ducts increase the release of aldosterone
decreased heart rate (yes) inhibition of Na/K ATPase increased calcium inside heart muscle increase formation of actinomyosin
blockade of beta receptors increased force of myocardial contraction blockade of alpha-1 receptors blockade of beta receptors and blockade of alpha-1 receptors
hydralazine (Apresoline) furosemide (Lasix) metoprolol (Lopressor) hydrochlorothiazide (HyroDIURIL)
untreated hypertension weakening of contractile force myocardial infarction valvular defects
eplerenone torsemide triamterene chlorothiazide
veins arteries the SA node myocardial contraction
slowing the heart rate increasing the release of renin increasing ADH increasing aldosterone
can be used in the treatment of refractory heart failure antagonize antidiuretic hormone at the receptors in the collecting duct block carbonic anhydrase in the loop of Henle, causing hypochloremic alkalosis waste potassium at doses that cause diuresis
hyperuricemia (excess of uric acid in the blood) hyperkalemia hypernatremia hypercalcemia
can cause hyperuricemia can cause hyperglycemia can be used to reduce ascites due to malignancy can cause metabolic acidosis
the proximal tubule the loop of Henle the distal tubule the capsule area of glomerular filtration
thiazide diuretics chlorthalidone isosorbide mononitrate triamterene
sodium uric acid water potassium
anuria is a state where no urine is formed the major tubular secretory function of the nephron involves hydrogen and potassium ions uremia is an accumulation of nitrogen waste products tubular reabsorption of water is diuresis
produce a mild diuresis without acid/base disturbance inhibit aldosterone receptors produce hypokalemia produce similar adverse effects to thiazide diuretics
movement of small molecules into the glomerulus nephron production of calcium carbonate transport of ions into the blood movement of sodium ions into circulation
glomerulus proximal convoluted tubule and collecting ducts distal convoluted tubule uremic channel
tubular secretion of hydrogen ions increasing the pH of the urine neutralizing cell waste products decreasing the production of bicarbonate ions
decrease in heart rate decrease in release of renin decrease in cardiac output only decrease in heart rate and decrease in cardiac output
reduction of blood volume blockade of alpha adrenergic receptors relaxation of vascular smooth muscle only reduction of blood volume and relaxation of vascular smooth muscle
alpha-blockers beta-blockers angiotensin-converting enzyme inhibitors angiotensin receptor blockers
verapamil propranolol prazosin captopril
hydralazine clonidine diltiazem losartan
activation of RNA mechanism vasodilation water excretion decreased blood pressure
increasing peripheral resistance increasing cardiac output increasing excretion of sodium only decreasing blood volume and increasing excretion of sodium
decreasing sympathetic nerve activity stimulating inhibitory alpha-2 receptors decreasing release of renin decreasing sympathetic nerve activity and decreasing release of renin
coronary artery disease CHF supraventricular arrhythmias coronary artery disease and supraventricular arrhythmias
macrophage B-cell helper T-cell killer T-cell
azathioprine cyclosporine cyclophosphamide infliximab
cyclosporine muromonab-CD3 cyclophosphamide mycophenolate
sargramostim infliximab interleukin-2 daclizumab
release interleukins produce antibodies provide long-term immunity recognize foreign antigens
killer T-cells B-cells memory cells killer T-cells and memory cells
reduce the number of T- and B-cells increase the number of lymphocytes in the blood inhibit synthesis of inflammatory mediators reduce the number of T- and B-cells and inhibit synthesis of inflammatory mediators
lefazathioprine cyclophosphamide cyclosporine mycophenolate mofetil
multiple sclerosis hairy cell leukemia lymphoma multiple sclerosis and lymphoma
inhibits dihydroorotate dehydrogenase, leading to inhibition of pyrimidine synthesis. inhibits inosine monophosphate dehydrogenase, the rate limiting enzyme in the formation of guanosine. inhibits the phosphatase activity of calcineurin, a cell-signaling protein that mediates T-cell activation. inhibits mTOR, a regulator of protein translation.
cyclosporine. sirolimus. mycophenolate mofetil. leflunomide.
etanercept. OKT3. rituximab. efalizumab.
systemic infection may occur in patients who are receiving drugs to suppress their immune system warts are an example of a dermatophytic fungal infection the majority of antifungal drugs interfere with fungal cell-wall integrity amphotericin B is associated with serious renal toxicity
piperacillin vancomycin gentamicin clindamycin
erythromycin tetracycline gentamicin clindamycin
lipid soluble well absorbed orally poorly absorbed from the GI tract and excreted mostly unchanged in the urine if injected devoid of serious adverse effects
binds to keratin is fungicidal forms ergosterol in hair and nails incorporates itself into fungal RNA
echinocandins inhibit polysaccharide (glucan) synthesis in the cell wall flucytosine binds to the cell membrane ticonazole is an antimetabolite for fungal RNA amphotericin B binds to a cytochrome P450-dependent enzyme
griseofulvin butenafine gentian violet clotrimazole
changing cell-wall synthesis binding to ergosterol inhibiting cell mitosis inhibiting neuraminidase
they are difficult to treat due to host cell invasion immunity can be gained through the attenuated live virus treatment can be given via an intranasal spray the vaccines are contraindicated in people allergic to eggs
mercaptopurine fluorouracil methotrexate cytarabine
doxorubicin asparaginase etoposide vincristine
tamoxifen anastrozole leuprolide goserelin
imatinib trastuzumab bevacizumab gefitinib
one of the early goals of chemotherapy is remission antineoplastic drugs only attack cancerous cells drug resistance is increased with combination therapy it is the primary form of treatment for solid tumors
preventing DNA replication blocking DNA synthesis forming abnormal nucleotides preventing DNA replication and forming abnormal nucleotides
bind irreversibly with nucleic acids decrease cells' ability to synthesize proteins are cell-cycle nonspecific bind irreversibly with nucleic acids and are cell-cycle nonspecific
they can bind to microtubules they induce enzymes they increase DNA strand breakage they can bind to microtubules, and they increase DNA strand breakage
Insulin aspart Insulin glargine Insulin glargine is a long-acting insulin analog designed to provide a slow and consistent release of insulin throughout the day and night. It is typically taken once daily to help manage blood sugar levels and provide basal insulin coverage.Insulin lispro Regular insulin
Autoantibody destruction of beta cells Type 1 diabetes is an autoimmune disorder in which the immune system mistakenly targets and destroys the insulin-producing beta cells in the islets of Langerhans within the pancreas.Malformed beta cells Failure of target tissue to respond to insulin Hyperinsulinemia
Male over the age of 45 Smoker Hypothyroidism Elevated HDL levels
is synthesized in the liver enters the body as dietary cholesterol is transported as chylomicrons in the blood is transported as HDL
it is a high-density lipoprotein high levels of LDL contribute to atherosclerosis it is a lipoprotein it contains more fat and less protein than "good cholesterol"
cholesterol is lowered by a diet rich in saturated fats cholesterol is elevated in people with primary hypercholesterolemia nicotinic acid is used to treat hyper cholesterolemia fenofibrate primarily affects VLDL and triglycerides
essential for building cell membranes needed to help form myelin sheath helps in digestion of dietary fats inhibits formation of nerve covering
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