Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
142 Cards in this Set
- Front
- Back
|
What stage of anesthesia is associated with excitement, delirium, combative behavior, and nightmares?
|
Stage II
|
|
|
What is the definition of general anesthesia?
|
analgesia, amnesia, loss of consciousness, inhibition of sensory and autonomic reflexes, and skeletal muscle relaxation
|
|
|
True of false: blood acts as an inactive reservoir that must be saturated before equilibrium is achieved.
|
True
|
|
|
True or false: the more soluble an anesthetic is in blood, the more potent it is, leading to a slower induction.
|
False, the more soluble, the more potent, but this leads to a SLOWER induction because you must first saturate the blood proteins (mainly albumin)
|
|
|
True or false: you need more of a poorly soluble general anesthetic to induce anesthesia.
|
True (1 MAC for sevoflurane/isoflurane/desflurane correlates to a higher mmHg mixture than that of methoxyflurane)
|
|
|
True or false: a general anesthetic with a higher MAC percentage may cause more drowsiness than a lower MAC percentage.
|
False, direct opposite
|
|
|
True or false: the equilibration between alveolar partial pressure of a general anesthetic and the arterial partial pressure does not depend on the particular anesthetic used.
|
False, it does play a large role
|
|
|
True or false: the equilibration between arterial and brain partial pressure of a general anesthetic does not depend on the particular anesthetic used.
|
True
|
|
|
What factor of MAC is generally used for surgeries?
|
1.3 x MAC (MAC is the minimum alveolar concentration necessary to prevent movement in response to surgical skin incision in 50% of patients)
|
|
|
True or false: MAC x Oil/Gas Partition Coefficient = 1.3?
|
Round about, yes
|
|
|
Name the four factors affecting the MAC of a general anesthetic.
|
Age (older has lower MAC), Body temperature (lower has a lower MAC; think of the temperature of an OR), Drug status (a sober drunk or meth head need a higher MAC; a drunk or high person need a lower MAC), and barometric pressure (higher altitudes need a higher MAC)
|
|
|
Name factors that do NOT affect the MAC of a general anesthetic.
|
Duration of administration
Biotransformation Sex Blood Pressure Arterial oxygenation Level of ventilation Hemoglobin concentration |
|
|
True or false: you require the [same] of general anesthetic in the lipid bilayer to achieve anesthesia.
|
True, you just need different doses of the general anesthetic to achieve that (due to different Oil/gas partition coefficient)
|
|
|
How do general anesthetics work in the brain?
|
Enhance GABA and inhibit excitatory receptors (e.g. glutamate receptors)
|
|
|
What happens to the following with under general anesthesia: tial volume, respiratory rate, minute ventilation, arterial PCO2, ventilatory response to CO2, and ventilatory response to hyposemia?
|
tial volume (decrease)
respiratory rate (increase) minute ventilation decrease) arterial PCO2 (increase) ventilatory response to CO2 (decrease) ventilatory response to hyposemia (abolished) |
|
|
Why is NO2 so commonly mixed with general anesthetics?
|
It does not alter our response to increased arterial PCO2, it maintains arterial pressure, and it offers some pain relief.
|
|
|
Which general anesthetic is chose for patients with a high intracranial pressure?
|
Isoflurane
|
|
|
True or false: as you increase the oil/gas partition coefficient, you increase the biotransformation by the liver and excretion through the kidney.
|
True
|
|
|
About what percentage of methoxyflurane is metabolized by the liver?
|
50% (higher oil/gas partition coefficient)
|
|
|
Sevoflurane has 3% metabolizaton. Would you want to use this general anesthetic for a long procedure?
|
No, the fluoride ions build up.
|
|
|
What leads to a decreasing effect of thiopental after administration?
|
Redistribution (highly lipid soluble)
|
|
|
Which general anesthetic is used to displace endogenous GABA inhibitors?
|
Etomidate
|
|
|
What category of drug is meprobamate?
|
Sedative-hypnotic
|
|
|
What determines the termination of the drug's action for the following categories of barbiturates: Thiopental (ultra-short-acting), Secobarbital/Pentobarbital (short-acting), and Phenobarbital (long-acting)?
|
Redistribution with 99% metabolism (15 minute action)
Metabolism and renal excretion No metabolism with full excretion These all deal with the correlation between lipid solubility and metabolism |
|
|
What is the main SE associated with barbiturate overdose?
|
Depression of the medullary respiratory center
|
|
|
What does and does not change as far as tolerance with barbiturates?
|
Does change: sedative-hypnotic
Does not change: anticonvulsant effect and respiratory depression |
|
|
What are the major signs of withdraw from barbs/benzos/alcohol?
|
Convulsions, delirium and death
|
|
|
Name three short acting benzos.
|
Triazolam, Midazolam, and Alprazolam (Xanax)
|
|
|
What chemical modification occurs with every benzodiazepine?
|
Glucuronidation (inducible by microsomal enzyme induction)
|
|
|
Name the only benzo used for skeletal muscle relaxation.
|
Diazepam (Valium)
|
|
|
Name a benzo very useful for panic attacks.
|
Alprazolam (Xanax)
|
|
|
Name three non-life threatening SE of benzos for hypnotic use.
|
Nightmares, tolerance, and abstinence syndrome (rebound insomnia)
|
|
|
What dose of benzos must you take in order to achieve coma?
|
None, that we learned (safe for suicidal patients)
|
|
|
Why are benzos not good for anticonvulsant use?
|
You develop a tolerance, unlike with barbs.
|
|
|
Buspirone: MOA, indication, bonuses
|
enhance 5-HT1A receptors; General anxiety disorder; no sedation, addiction, tolerances, or interaction with alcohol
|
|
|
What is Zolpidem, and what is its MOA?
|
Ambien (sleep aid); it works on benzo receptors (small tolerance)
|
|
|
What is Eszopiclone, and what is its MOA?
|
Lunesta (sleeping aid); it works by mimicking benzos (shows no tolerance)
|
|
|
What is Flumazenil
|
Benzodiazepine receptor antagonist (takes 5-10 minutes and may precipitate a seizure)
|
|
|
How long does it take for Buspirone to take effect? Is this different than most other benzodiazepines?
|
It takes a couple weeks to work. Most other benzodiazepines work very quickly.
|
|
|
Which benzo is commonly known to cause withdrawal symptoms of rebound insomnia?
|
Triazolam
|
|
|
Which lab procedures must you take into account when evaluating a poison-overdose patient?
|
Arterial blood gases
Electrolytes (anion gap, normally 12 - 16 mEq/L) Renal function tests Serum osmolality (normal zero gap) EKG |
|
|
What three signs contraindicate induction of emesis/gastric lavage in poisoned patient?
|
Seizures, absence of gag reflex, and ulcerated oral mucous membranes.
|
|
|
Should ipecac be simultaneously administered with charcoal or catharsis?
|
NO, they will bind together
|
|
|
What four toxins can easily be removed with hemodialysis?
|
Ethylene glycol, lithium, methanol, and salicylate
|
|
|
What is Fomepizole?
|
It inhibits alcohol dehydrogenase.
|
|
|
What are the top two pollutants?
|
CO2, CO
|
|
|
Are chelating agents nucleophiles or electrophiles?
|
Nucleophiles (they donate electrons to heavy metals)
|
|
|
Upon lead exposure, which two enzymes are inhibited, and which compound builds up?
|
Delta-aminolevulinate dehydrogenase and Ferrochelatase
Delta-aminolevulinate builds up |
|
|
What is the short term, and long term treatments of lead exposure?
|
EDTA for short term
Penicillamine for long term |
|
|
What is the short term, and long term treatments of arsenic exposure?
|
Gastric lavage/catharsis for short term exposure
BAL for long term exposure |
|
|
What are three side effects of arsenic exposure?
|
Rice water stools and vomiting, BM depression, and uncoupling of oxidative phosphorylation
|
|
|
Mercury exposure: acute exposure treatment? Chronic exposure treatment?
|
BAL (inorganic mercury)
No good chronic exposure treatment to organic mercury exposure |
|
|
What are somatomedins, where do they come from, and what is an example?
|
Somatomedins are the business end of growth hormone.
They are made from the liver in response to GH stimulation IGF-1 (Insulin-like growth factor 1) |
|
|
True or false: Dopamine agonist (bromocriptine, L-DOPA, and Ropinrole) will stimulate GH release.
|
Very true
|
|
|
What are three responses to GH?
|
Increased amino acid uptake and storage by myocytes, increased fat use for energy, and gluconeogenic
|
|
|
What endogenous molecule and its chemical cousin result in decreased GH release?
|
Somatostatin and Ocreotide
|
|
|
What three indications does Ocreotide have?
|
Inhibiting GH release, treating a nasty secretory diarrhea, and ESOPHAGEAL VARICES
|
|
|
True or false: prolactin does not have a correlation with breast cancer.
|
False
|
|
|
What five things stimulate the release of prolactin?
|
PRH (TRH), opiates, estrogens, stress, and exercise
|
|
|
Can people on high doses of antipsychotic drugs conceive a child?
|
No, the DA antagonist allows a high prolactin release from the pituitary gland, which inhibits release of FSH/LH
|
|
|
What are three compounds that can inhibit the release of corticosteroids.
|
Aminogluthemide (blocks cholesterol to pregnenolone step), ketoconazole (inhibits 17 alpha-hydroxylase), and metyrapone (inhibits 11 beta-hyroxylase)
|
|
|
What two things mainly manage the mineralocorticoid pathway?
|
Potassium levels and AT II
|
|
|
What is the pharmacologic compound for ACTH?
|
Cosyntropin
|
|
|
What fraction of endogenous Cushing's disease is from a pituitary adenoma?
|
2/3
|
|
|
Name five treatments for Cushing's syndrome.
|
Adrenalectomy
Aminogluthethemide Mitotane (pharmacological adrenlectomy) Metyrapone Ketoconazole |
|
|
What is the chemical agent used to destroy the adrenal gland?
|
Mitotane
|
|
|
What is the chemical agent used to destroy the adrenal gland?
|
Mitotane
|
|
|
What is the chemical agent used to destroy the adrenal gland?
|
Mitotane
|
|
|
When should you use corticosteroids for treatment?
|
When other treatments have failed
|
|
|
Can corticosteroids be used to treat hypercalcemia?
|
Yes; glucocorticoids act as physiologic antagonists of vitamin D
|
|
|
What is a common GI negative SE of corticosteroids?
|
GI ulceration due to decrease production of protective PGs (inhibition of PLA decreases PG synthesis)
|
|
|
Recapitulate the link between between glucocorticoids and osteoporosis.
|
Glucocorticoids inhibit both vitamin D (decrease intestinal absorption of calcium) and osteoblast action. The resulting hypocalcemia increases PTH, which increases the activity of osteoclasts, leading to osteoporosis!!!
|
|
|
How much glucocorticoid activity does fludrocortisone have? Dexamethasone?
|
Fludrocortisone has NO glucocorticoid activity, whereas dexamethasone has full glucocorticoid activity with no mineralocorticoid activity (reverse of above)
|
|
|
What form of insulin is stored within the pancreas? How about most commercial preparations of insulin?
|
Both use the hexameric form
|
|
|
How many units of insulin are found in one mg?
|
25 units/mg
|
|
|
What is the MOA of sulfonylreas?
|
They inhibit the K+ channels in the pancreatic Beta cells, leading to a depolarization, which opens in the Ca-channels, letting in calcium, which allows the fusion of insulin-storage vesicles to dock and release their insulin into the bloodstream
|
|
|
True or false: insulin increases TG and VLDL formation.
|
True, but they also upregulate LPL activity on adipocytes, leading to increased uptake and storage
|
|
|
What is the MOA behind increased TG levels in diabetics?
|
Their LPL enzyme on adipocytes is not active, so they can't catch the circulating TGs found within the VLDL molecules
|
|
|
Which type of diabetes has a stronger familial component?
|
Type II
|
|
|
Which type of diabetes is associated with amyloid deposition within pancreatic Beta cells?
|
Type II
|
|
|
Which type of diabetes is associated with HLA isotypes?
|
Type I
|
|
|
What is NPH insulin?
|
It is a protamine in phosphate buffer of insulin, whereby enzymes slowly degrade protamine thereby liberating the insulin.
|
|
|
What is the onset/DOA for NPH insulin?
|
Onset 1.5 hours (intermediate) with 16-24 hour DOA (peak at 4-10 hours)
|
|
|
What is Lispro? Peak? DOA?
|
Ultrarapid-acting insulin
20 minutes to onset 1 hour peak lasts 3-4 hours |
|
|
What is regular insulin?
|
Onset in 40 minutes, with peak in 2-3 hours, and lasts 6-8 hours (everything is double that of Lispro, and 1/2 to 1/3 that of NPH insulin)
|
|
|
What is Glargine?
|
Long acting insulin
4-6 hours to onset with NO peak Lasts 18-24 hours |
|
|
What is special about Glargine?
|
Since aas have been moved around and added, this insulin analog is soluble at pH 4.0. This forms a precipitate at physiological pH (7.4), leading to a much slower onset
|
|
|
How can giving a Beta-blocker to a diabetic make the condition worse?
|
It will inhibit the Beta-2 receptors in the Beta cells, leading to a decrease in insulin output, in addition to the inhibition of Beta-1 cells in the alpha cells, leading to a decrease in glucagon output (leading to hypoglycemia with decreased insulin output)
|
|
|
Name two second generation sulfonylureas, and describe how they differ from the first generations.
|
Glyburide and Glipizide; second generations are more potent, and therefore require a much lower dose.
Note: both generations of sulfonylureas are hypoglycemic-inducing drugs |
|
|
Name two functions of metformin?
|
Increase peripheral response to insulin and decreases gluconeogenesis of liver
|
|
|
What is the MOA of acarbose?
|
Inhibits brush border alpha-glucosidase
|
|
|
Name three TZDs, and MOA.
|
Troglitasone, Rosiglitazone, Pioglitazone
Stimulates PPARs, leading to increased insulin response in adipocytes, myocytes, and liver |
|
|
What are the toxicities associated with the TZDs?
|
Troglitazone (removed due to idiosyncratic liver toxicity)
Rosiglitazone (increased CHF) Use Pioglitazone |
|
|
What is Exenatide, and what is the MOA?
|
It is a synthetic incretin (GLP-1) that increases insulin output and decreases glucagon output.
|
|
|
What is Sitagliptin (Januvia)? MOA?
|
Inhibits dipeptidyl peptidase IV, which leads to a decrease in the degradation of incretin.
Nice oral dosing, lower efficacy than exenatide though |
|
|
Name two compounds that inhibit uptake of iodine into the thyroid gland.
|
Perchlorate and Thiocyanate
|
|
|
Is thyroid hormone an example of a protein or a steroid hormone?
|
Neither
|
|
|
Which hormone receptor is associated with the retinoic acid receptor (RXR)?
|
Thyroid hormone displaces the corepressor from the thyroid hormone-RXR complex to allow transcription of thyroid specific genes.
|
|
|
True or false: thyroid hormone's effect depends upon protein synthesis as well as potentiation of the secretion and action of growth hormone.
|
True
|
|
|
Which two hormones/endogenous compounds (that we have talked about) increase the sensitivity to catecholamines?
|
Cortisol and thyroid hormone
|
|
|
What is one of the top treatments for hyperthyroidism?
|
Beta-blockers
|
|
|
What form of thyroid hormone (D or L) can be utilized to lower cholesterol levels?
|
D
|
|
|
Name two antithyroid drugs that act be inhibiting organification of iodide, blocking the coupling of iodotyrosine, and interfere with the peripheral deiodination of T4 to T3.
|
Propylthiouracil and methimazole
|
|
|
Name three functions of excess iodide ion on the thyroid gland.
|
Inhibit organification, hormone release, and decrease size and vascularity of the hyperplastic gland.
|
|
|
Which Iodide ion is used to "melt" the thyroid?
|
I 131 (I 123 used for scans)
|
|
|
What percentage of patients treated with radioactive iodide (I 131) is cured by a single dose?
|
50-60%
|
|
|
Which two locations of the body are often times associated with osteoporitic fractures, and why?
|
Neck of femur and vertebral bodies. These two locations have a lot of trabecular bone.
|
|
|
True or false: 1,25-Dihyroxycalcitriol potentiates/enhances the bone's response to PTH, leading to bone reabsorption.
|
True
|
|
|
True or false: PTH has no action in depositing calcium into bone.
|
False (Dr. Z argument with coworker)
|
|
|
Name the two I.V. phosphates used to increase bone mineralization.
|
Pamidronate and Zolendrolate
|
|
|
True or false: renal failure patients often times get hypercalcemia.
|
False: they get hypocalcemia because they cannot excrete PO4, so the calcium*phosphate constant drives calcium and phosphate into bone.
|
|
|
What is a good treatment for psdudohypoparathyroidism?
|
A lot of calcium by mouth to bind and cause catharsis of phosphate.
|
|
|
Name three compounds that stimulate osteoblasts to express the RANKL.
|
PTH, shear stress, and TGF-Beta
|
|
|
What is the MOA of bisphosphanates.
|
The bisphosphanates bind to the hydroxyapatite crystal, and inhibits osteoclasts upon ingestion of the crystal. Any drug that ends in -dronate is a bisphosphanate (IV and oral forms)
|
|
|
True or false: you get uterine bleeding and breast tenderness with raloxifene.
|
False (you only get leg cramps and HOT FLASHES)
|
|
|
Estrogen at high levels can lead to infertility. This occurs through inhibition of the hypothalamus, preventing the release of LHRH. Which drug is able to inhibit the negative feedback of estrogen, leading to bountiful excretion of LHRH, FSH, and LH?
|
Clomiphene (multiple births abound)
|
|
|
How long should you use clomiphene for infertility use?
|
7-10 days
|
|
|
What percentage of patients taking clomiphene have multiple births?
|
8%
|
|
|
If someone is LH/FSH deficient (therefore cannot treat with clomiphene), how can you surpass infertility issues?
|
Use menotropins (urine from menopausal women (have high levels of LH/FSH), but use FSH only)
plus HCG from pregnant women (acts like LH surge) |
|
|
Name two "super LHRH" agonists, and explain their use.
|
Nafaralin + leuproline
These are used to pound away at the LHRH negative feedback regulator, leading to decreased LH/FSH release This can be used to treat endometriosis and prostate cancer! |
|
|
Name two endocrine drugs that can treat prostate cancer through the action of LHRH negative feedback.
|
Nafaralin and Leuprolide
|
|
|
Name three drugs that can be utilized to fight breast cancer after surgical removal.
|
Tamoxifen, Raloxifene, and Clomiphene
|
|
|
True or false: estrogen leads to salt and water retention.
|
True
|
|
|
True or false: estrogen leads to a decrease in LDL and an increase in HDL.
|
True (progesterone is the exact opposite)
|
|
|
Name two synthetic estrogens that are resistant to hepatic degradation.
|
Mestranol and ethinyl estradiol
|
|
|
True or false: women put on oral contraceptives will suffer from impaired glucose tolerance from the estrogens.
|
True
|
|
|
Name four pharmacological agents that target the alpha receptors of the prostate/neck of the bladder that assist in increased urine flow.
|
Terazosin, doxazosin, prazosin, and TAMSULOSIN
|
|
|
Name the drug that inhibits 5-alpha reductase, resulting in decreased prostate size.
|
Finasteride
|
|
|
Name the competitive inhibitor of dihydrotesterone.
|
Bicalutamide
|
|
|
Why does increased lactate lead to hyperuricemia?
|
Both urate and lactate compete for the some excretion port in the PCT.
|
|
|
Which benzodiazepine is used to alleviate withdrawal symptoms of ethanol?
|
Chlorodiazapoxide
|
|
|
Name the compound that inhibits acetaldehyde dehydrogenase, leading to negative side effects of drinking?
|
Disulfiram
|
|
|
Name the compound that inhibits alcohol dehydrogenase.
|
Fomepizole
|
|
|
True or false: apolipoproteins provide structural stability to the lipoprotein particle and act as ligands for specific cell surface receptors or as cofactors for enzymatic reactions.
|
True as can be
|
|
|
What causes diabetics to have such high triglyceride levels?
|
Their LPL activity in peripheral tissues is so low (no insulin guided activity)
|
|
|
What is the first step in management of patients with hyperlipoproteinemias?
|
Diet
|
|
|
Niacin: MOA, SE
|
Niacin inhibits HSL in peripheral tissues, leading to decreased FFAs.
This leads to a decrease in VLDL/LDL Niacin also increases HDL through the increased synthesis of ApoAI Facial flushing (give aspirin before) |
|
|
Name two fibrates, and describe their MOA.
|
Gemfibrozil and Fenofibrate
Activates PPAR-alpha, ultimately leading to a 50% reduction in plasma triglycerides (decreases apoCIII synthesis, increases apoAI/II synthesis, and increases FA oxidation in hepatocytes) |
|
|
Name two bile acid-binding resins, and describe the outcome.
|
Cholestyramine and Colestipol
Lower plasma LDL by 20% (increase hepatic LDL receptors, but also increase HMG CoA reductase activity) |
|
|
Statins: examples and MOA
|
Lovastatin, simvastatin, pravastatin (no fibrate interaction), atorvastatin (Lipitor), and rosuvastatin (Crestor)
Inhibits action of HMG CoA reductase by mimicking a half-reduced intermediate All but pravastatin are metabolized by the CYP3A4 family, which is also inhibited by the fibrates (especially a problem with gemfibrozil) |
|
|
Name three side effects of statins.
|
Rhabadomyolysis (dose-related), with sequential renal failure (nephron hates myoglobin), and increased liver serum transaminases (perform LFTs)
|
|
|
Name the cholesterol lowering agent that works by inhibiting the absorption of cholesterol by the small intestine.
|
Ezetimibe (could potentially be cholestyramine and/or colestipol)
|
