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;
413 Cards in this Set
- Front
- Back
Essential HTN
|
Diuretics
ACE-I's ARBs CCB |
|
CHF
|
Diuretics
ACE's/ARB's Beta blockers (for compensated CHF) K+ sparing diuretics |
|
Diabetes Mellitus
|
ACE/ARB
CCB Diuretics Beta blockers Alpha blockers |
|
Hydralazine MOA
|
increase cGMP --> sm muscle relaxation.
Vasodialates arterioles > veins. dec afterload |
|
Hydralazine uses
|
Severe HTN, CHF.
First line for HTN in pregnancy with methyldopa. coadmin'd with beta blocker to block reflex tachy |
|
Hydralazine SE
|
Compensatory tachy (contraindicated in angina/CHF), fluid retention, nausea, HA, angina. SLE-like syndrome
|
|
CCBs
|
Nifedipine
Verapamil Diltiazem |
|
CCB MOA
|
Block voltage dependent L-type Ca++ channels of cardiac and smooth muscle thereby reducing muscle contractility.
|
|
CCB uses
|
HTN, angina, arrythmias (not nefedipine), Raynauds
|
|
CCB toxicity
|
Cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation
|
|
Nitroglycerine
Isosorbide dinitrate MOA |
Vasodilate by releasing NO in smooth muscle causing inc cGMP and smooth muscle relaxation
Dialates veins > arteries (versus hydralazine) Dec preload |
|
Nitroglycerine
Isosorbide dinitrate USES |
Angina, pulmonary embolus
Aphrodisiac and erection enhancer |
|
Nitroglycerine
Isosorbide dinitrate TOXICITY |
Reflex tachy, hypotension, flushing, HA
Monday disease in industrial exposure = dvlp tolerance to vasoD effects during the work week and loss of tolerance during weekend. reexposure on Monday = tachy, dizziness and HA. |
|
Malignant HTN txmnt
(3 drugs) |
1. Nitroprusside
2. Fenoldopam 3. Diazoxide |
|
Nitroprusside
|
Short acting
inc cGMP via direct release of NO Can cause cyanide toxicity (because it releases CN) |
|
Fenoldopam
|
Dopamine D1-R agonist
Relaxes renal vasculature smooth muscle |
|
Diazoxide
|
K+ channel opener = hyperpol and relaxes vascular smooth muscle.
Can cause hyperglycemia (because it reduces insulin release) |
|
Hydralazine in a nutshell
|
inc cGMP
relaxes arterioles > veins dec afterload |
|
Nitro in a nutshell
|
inc cGMP
relaxes veins > arteries dec preload |
|
What is the goal of anti-anginal therapy?
|
Reduction of myocardial O2 consumption by decreasing 1 or more determinants of myocardial O2 consumption.
|
|
What are the determinants of myocardial O2 consumption?
|
1. EDV
2. BP 3. HR 4. Contractility (inotropy) 5. Ejection fraction (>55% = healthy) |
|
Niacin SE
|
Flushing (dec by aspirin or long-term use)
Hyperglycemia (acanthosis nigricans) Hyperuricemia (exacerbates gout) |
|
Bile acid resins
|
1. cholestyramine
2. colestipol 3. colesevelam |
|
Bile acid resin SE
|
-Patients hate them because they taste bad and cause GI discomfort
-dec absorption of fat soluble vitamins (DAKE) -cholesterol gallstones |
|
cholesterol absorption blockers
(it's EZ to remember, silly!) |
EZetimibe
|
|
Cholesterol absorption blocker SE
|
Rare inc LFT
|
|
Fibrates
|
1. gemFIBrozil
2. cloFIBrate 3. benzFIBrate 4. fenoFIBrate |
|
Fibrates SE
|
Myositis
hepatotoxicity (inc LFTs) cholesterol gallstones |
|
Niacin MOA for controlling lipid levels
|
Inhibits lipolysis in adipose tissue
Reduces hepatic VLDL secretion into circulation |
|
Bile acid resins MOA
|
prevent intestinal reabsorption of bile acids so the liver must use cholesterol to make more.
|
|
cholesterol absorption blockers site of action
|
prevent cholesterol reabsorption at small intestine brush border.
|
|
fibrates MOA
|
upregulate LPL --> inc TG clearance
|
|
Do beta blockers inc or dec contractility?
|
Dec.
Beta-1-R are Gs and activate protein kinase A which phosphorylates L-type Ca++ channels and phospholamban, both of which inc intracellular Ca++ during contraction = inc contractility. So blocking the beta-1's will dec contractility. |
|
Cardiac glycosides
|
Digoxin
Urinary excretion |
|
Digoxin MOA
|
Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca++ exchanger/antiport. This leads to inc intracellular Ca++ and positive inotropic effect (inc contractility). Also stim vagus nerve.
|
|
Digoxin
USES |
CHF (inc contractility)
a. fib (dec conduction at AV node and depresses SA node) |
|
Digoxin
TOXICITY |
cholinergic = n/v, diarrhea, BLURRY YELLOW VISION
ECG = inc PR, dec QT, T wave inversion, arrhythmia, hyperK+ |
|
What exacerbates digoxin toxicity?
|
Renal failure (dec excretion)
HypoK+ (makes it easier for dig to bind at K+ binding site on Na+/K+ ATPase) Quinidine (dec digoxin clearance; displaces dig from tissue binding sites) |
|
Antidote for digoxin intoxication
|
Slowly normalize K+
Lidocaine Cardiac pacer Anti-dig Fab fragments Mg2+ |
|
Class I antiarrhythmics
|
Na+ channel blockers
Local anesthetics Slow/block conduction Dec slope of phase 0 depol and inc threshold for firing in abnorm pacemaker cells. |
|
Class 1A
|
Quinidine
Procainamide Disopyramide |
|
Class 1A
MOA |
INCREASE AP duration
inc ERF inc QT interval |
|
Class 1A
USES |
Atrial and ventricular arrhythmias, esp reentrant and ectopic SVT and V tach
|
|
Class 1A
TOX |
Quinidine = cinchonism
Procainamide = reversible SLE-like All = Thrombocytopenia Torsades (due to inc QT) |
|
Class 1B
|
Lidocaine
Mexiletine Tocainamide |
|
Class 1B
USES |
Acute ventricular arrythmias (esp post-MI)
Digitalis induced arrythmias |
|
Class 1B
MOA |
DECREASE AP duration
Preferentially affect ischemic or depol'd Purkinje and ventricular tissue. |
|
What e'lyte imbalance causes inc toxicity for all class 1?
|
Hyperkalemia
|
|
pneumonic for 1B versus 1C:
|
1B = Best for post-MI
1C = Contraindicated post-MI |
|
Class II antiarrhythmics
|
Beta blockers!
"--olol" |
|
B-blockers
MOA |
dec cAMP
dec Ca++ currents Suppress abnormal pacemakers by dec slope of phase 4 AV node is particularly sensitive = inc PR interval |
|
B-Blockers
USES |
V-tach
SVT Slow ventricular rate duing a.fib and a.flutter |
|
B-Blockers
TOX |
Impotence, exacerbation of asthma, CV effects (brady, AV block, CHF), CNS effects (sedation, sleep dist)
**May mask hypoglycemia |
|
B-Blockers
Antidote |
Glucagon
|
|
What B-blocker is very short acting?
|
Esmolol
|
|
What B-blocker can also be used for dyslipidemia?
|
Metoprolol
|
|
Do B-blockers affect preload or afterload?
|
Afterload
|
|
Class III antiarrhythmics
|
K+ channel blockers, silly!
SotAlol Amniodarone Ibutilide Bretylium Dofetilide |
|
Class III
USES |
Used when other antiarrhythmics fail
|
|
Class III
Amiodarone (40% iodine by weight) TOX |
Amiodarone = pulmonary fibrosis, hepatotoxcity, hypo/hyperthyroid. Check PFTs, LFTs, and TFTs when using. Corneal deposits, skin deposits (blue/gray) leads to photodermatitis, neuro effects, constipation, CV effects (brady, heart block, CHF)
Amniodarone alters the lipid membrane, so it has shit tons of SEs. |
|
Class III
SotAlol TOX |
Torsades, excessive beta blockade
|
|
Class III
MOA |
inc AP duration (like 1A)
inc ERP (like 1A) inc QT interval |
|
Class IV antiarrhythmics
|
CCB!
Verapimil Diltiazam |
|
Class IV
MOA |
dec conduction velocity
inc ERP (like 1A, class III) inc PR interval |
|
Class IV
USES |
prevention of nodal arrhythmias (like SVT)
|
|
Class IV
TOX |
flushing, constipation, edema, CV effects (CHF, AV block, SA depression)
|
|
Adenosine MOA
|
inc K+ our of cells --> hyperpol the cell and dec intracellular Ca++
|
|
Adenosine TOX
|
Flushing, hypotension, chest pain
|
|
Adenosine USES
|
DOC for diagnosing/abolishing SVT
Very short acting |
|
What drug blocks the effects of adenosine?
|
Theophylline
|
|
What metal is effective in torsades and digoxin toxicity?
|
Mg++
|
|
What e'lyte depresses ectopic pacemakers in hypokalemia (as seen in digoxin toxicity)?
|
K+
|
|
MEN 1
(Wermer's syndrome) |
3 P's
Pancreas Pituitary Parathyroid |
|
MEN 2A
(Sipple's syndrome) ret gene |
2 P's
Pheochromocytoma Parathyroid |
|
MEN 2B
ret gene |
1 P
Pheochromocytoma Marfinoid body habitus |
|
Insulin SE
|
Hypoglycemia
HSR (rare) |
|
Sulfonylureas
|
1st gen: tolbutamide, chlorpropamide
2nd gen: glyburide, glimepiride, glipizide |
|
Sulfonylureas MOA
|
close K+ channels in beta cell membrane, so cell depolarizes --> triggering of insulin release via inc Ca++ influx
|
|
Sulfonylureas USES
|
stimulate the release of endogenous insulin in DM-2
requires some islet cell fxn, so it is not useful in DM-1 |
|
Sulfonylureas TOX
|
1st gen = disulfram like rxns
2nd gen = hypoglycemia |
|
Biguanides
|
Metformin
|
|
Biguanide MOA
|
exact MOA unknown
dec gluconeogenesis inc glycolysis inc peripheral glucose uptake |
|
Biguanide USES
|
Oral
Can by used in pt's with no islet fxn |
|
Biguanide TOX
|
most serious = lactic acidosis
contraindicated in renal failure |
|
Glitazones/thiazolidinediones
|
Pioglitazone
Rosiglitazone |
|
Glitazones/thiazolidinediones
MOA |
inc insulin sensitivity in peripheral tissues.
binds to PPAR-gamma nuclear transcirption regulator |
|
Glitazones/thiazolidinediones
USES |
Used as monotherapy in DM-2 or combined with insulin, sulfonylureas or biguinide
|
|
Glitazones/thiazolidinediones
TOX |
Weight gain, edema, hepatotox, CV tox
|
|
alpha-glucosidase inhibitors
|
Acarbose
Miglitol |
|
alpha-glucosidase inhibitors
MOA |
Inhibit intestinal brush border alpha-glucosidases. Delayed sugar hydrolysis and glucose absorption = dec post-prandial hyperglycemia
|
|
alpha-glucosidase inhibitors
USES |
Used as monotherapy or combined for DM-2
|
|
alpha-glucosidase inhibitors
TOX |
GI disturbances
|
|
Mimetics
MOA USES TOX |
Pramlintide
MOA = dec glucagon USES = DM-2 TOX = hypoglycemia, nausea, diarrhea |
|
Propylthiouracil
Methimazole MOA USES TOX |
inhibit organification of iodide and coupling of thyroid hormone synthesis
USES = hyperthyroidism TOX = skin rash, agraulocytosis (rare), aplastic anemia Methimazole is teratogenic |
|
Levothyroxine
Triiodothyroxine |
MOA = thyroxine replacement
USES = hypothyroidism, myxedema TOX = tachy, heat intolerance, tremors, arrhythmias |
|
Growth hormone
USES |
GH deficiency, Turner's syndrome
|
|
Octreotide
USES |
= Somatostatin
Acromegaly, carcinoid, gastrinoma (Z.E.), glucagonoma |
|
Oxytocin
Clinical USES |
Stimulates labor, uterine contractions, milk let-down, controls uterine hemorrhage
|
|
Desmopressin
clinical USES |
= ADH
Pituitary (central, not nephrogenic) DI |
|
Demeclocycline
|
MOA = ADH antagonist
USES = SIADH TOX = nephrogenic DI, photosensitivity, abnormalities of bone and teeth |
|
Glucocorticoids
|
Hydrocortisone
Prednisone Trimcinolone Dexamethasone Beclomethasone |
|
Glucocorticoids
MOA |
decrease the production of leukotrienes and PGE's by inhibiting phospholipase A2 and expression of COX-2
|
|
Glucocorticoids
USES |
Addison's disease
Inflammation Immune suppression Asthma |
|
Glucocorticoids
TOX |
Iatrogenic Cushing's syndrome
Adrenal insufficiency when drug is d/c after chronic use. |
|
H2 blockers
|
"--dine"
cimetidine, ranitidine, famotidine, nazatidine |
|
H2 blockers MOA
|
Reversible blockade of histamine H2-R --> H+ secretion by parietal cells
|
|
H2 blockers USES
|
Peptic ulcers, gastritis, mild esophageal reflux
|
|
H2 blockers TOX
|
Cimetidine = potent inhibitor of p450
also has anti-androgenic effects (prolactin release, gynocomastic, impotence, dec libido in males) Can cross BBB and placenta Both cimetidine and ranitidine dec renal excretion of creatinine. |
|
PPIs
MOA USES |
"--prazoles"
MOA = irreversibly inhibits H+/K+ ATPase in stomach parietal cells USES = peptic ulcer, gastritis, esophageal reflux, ZE syndrome |
|
Bismuth, sucralfate
MOA USES |
MOA = binds to ulcer base, providing physical protection, allows HCO3- secretion to reestablish pH gradient in mucus layer
USES = inc ulcer healing, traveler's diarrhea |
|
What is the triple therapy of H.pylori ulcers?
|
1. Metronidazole
2. Amoxicillin (or tetracycline) 3. Bismuth Can also use a PPI. |
|
Misoprostol MOA
|
A PGE1 analog. Inc production and secretion of gastric mucous barrier. Dec acid production
|
|
Misoprostol USES
|
Prevention of NSAID-induced peptic ulcers
Maintain a ductus arteriosus Induces labor |
|
Misoprostol TOX
|
Diarrhea
Contraindicated in women of childbearing potential |
|
Muscarinic antagonists
|
Prenzepine
Propantheline |
|
Muscarinic antagonists
MOA |
Block M1-R on ECL cells (=dec histamine secretion) and M3-R on parietal cells (dec H+ secretion)
|
|
Muscarinic antagonists
USES |
Peptic ulcer (rarely used)
|
|
Muscarinic antagonists
TOX |
Tachy, dry mouth, difficulty focusing eyes
|
|
Octreotide
MOA USES TOX |
MOA = Somatostatin analog
USES = Acute variceal bleeds, acromegaly, VIPoma, carcinoid TOX = nausea, cramps, steatorrhea |
|
Infliximab
MOA USES TOX |
MOA = monoclonal AB to TNF (a proinflamm cytokine)
USES = Chron's disease, RA TOX = Respiratory infxn (eg reactivation of TB), fever, hypotension |
|
Sulfasalazine
|
MOA = a combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflam). Activated by colonic bacteria
USES = chron's and UC |
|
Ondansetron
|
MOA = 5-HT3 antagonist, powerful centrally acting antiemetic.
USES = control vomiting postoperatively and in chemo pts |
|
Metoclopramide
|
MOA = D2-R antagonist. Inc resting tone, contractility, LES tone, motility.
Does not influence colon transport time. USES = Diabetic and post-surgery gastroparesis |
|
Metoclopramide
TOX |
Inc parkinsonism effects
Contraindicated in pts with small bowel obstruction |
|
Hepabrin MOA
|
Cofactor for the activation of antithrombin, dec thrombin and X. Short half life.
|
|
Heparin TOX and Antidote
|
Bleeding and thrombocytopenia (HIT), osteoporosis.
Rapid reversal use protamine sulfate (positive charged molecule that binds neg charged heparin) |
|
Heparin USES
|
Immediate anticoagulation for PE, stroke, acute coronary syndrome, MI, DVT. Can be used in pregnancy
|
|
To follow heparin levels, use the __
|
PTT
|
|
Mechanism of HIT
|
hepatin binds factor IV, causing AB production that binds to and activates platelets leading to their clearance and resulting in a thrombocytopenic, hypercoag state
|
|
How is LMWH (enoxaparin) better than regular heparin?
|
Acts more on X, has better bioavailability and 2-4x longer half life. SubQ admin and no need for lab monitering. Not easily reversible.
|
|
Lepirudin
Bivalirudin |
Directly inhibit thrombin
Used as alternative to heparin for anticoagulating pts with HIT. |
|
Warfarin MOA
|
Inhibits epoxide reductase and vitamin K dependant factors (2, 7, 9, 10 and protein C and S).
Metabolized by cyp p450 |
|
How do you moniter Warfarin?
|
Effects on EXtrinsic pathway.
Moniter with PT/INR. (the EX-PresidenT went to WAR) |
|
Warfarin USES
|
Chronic anticoagulation
Not used in preggos (because warfarin, unlike heparin, crosses the placenta) |
|
Warfarin TOX and txment
|
Bleeding, teratogenic (category X), skin/tissue necrosis, drug-drug interactions.
To reverse warfarin, give vit K For rapid reversal of severe OD, give FFP |
|
Site of action for warfarin vs heparin:
|
Warfarin = Liver
Heparin = Blood |
|
Thrombolytics
|
Streptokinase
Urokinase tPA (alteplase) APSAC (anisteplase) |
|
Thrombolytics MOA
|
Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots.
Inc PT, inc PTT, no change in platelet count. |
|
Thrombolytics USES
|
acute MI, early ischemic strokes
|
|
Thrombolytic toxicity txmnt
|
Aminocaproic acid (inhibitor of fibrinolysis)
|
|
Thrombolytics TOX
|
Bleeding.
Contraindicated in active bleeding pts, hx of intracranial bleed, known bleeding disorders, severe HTN. |
|
Aspirin MOA
|
acetylates and irreversibly inhibits COX (1 and 2) to prevent conversion of arachidonic acid to thromboxane A2.
Inc bleeding time, no effect on PT/PTT |
|
Clopidogrel
Ticlopidine MOA |
Inhibit platelet aggregation by irreversibly blocking ADP-Rs. Inhibit fibrinogen binding by preventing GIIb/IIIa expression.
|
|
Clopidogrel
Ticlopidine USES |
Acute coronary syndrome, coronary stenting, dec incidence or recurrence of thrombotic stroke.
|
|
Ticlopidine TOX
|
neutropenia
|
|
Abciximab
MOA, USES, TOX |
MOA = Monoclonal antibody that binds to the GIIb/IIIa on activated platelets, preventing aggregation
USES = acute coronary syndromes, percutaneous transluminal coronary angioplasty TOX = bleeding, thrombocytopenia |
|
What cancer drug inhibits the M phase?
|
Vinca alkaloids and taxols
MOA of vinca= inhibit microtubule formation MOA of paclitaxol = inhibit microtubule disassembly |
|
What phase of the cell cycle does bleomycin inhibit and how?
|
G2 phase (=synthesis of materials needed for cell division)
MOA = combines with iron forming a complex that generates free radicals in presence of O2 |
|
What two phases does Etopside inhibit and how?
|
Phase G2 and S
MOA = inhibits topoisomerase II |
|
Alkylating agents (cisplatin) MOA
|
cross-link DNA
|
|
Dactinomycin
Doxorubicin MOA |
Intercalate DNA
|
|
Methotrexate MOA
|
Folic acid analog that inhibits DHFR --> dec dTMP (thymidine) --> dec DNA and protein synthesis
|
|
Methotrexate USES
|
Cancers: leukemia, lymphomas, choriocarcinoma, sarcomas
Non-neoplastic uses: abortion, ectopic pregnancies, RA, psoriasis |
|
Methotrexate TOX
|
1. myelosuppression which is reversible with leucovorin
2. Macrovesicular fatty change in liver 3. Mucositis 4. Teratogenic |
|
5-fluorouracil (5-FU)
MOA |
Pyrimidine analog
active metabolite complexes with folic acid. This complex inhibits thymidylate synthase --> dec dTMP = dec DNA and protein synthesis |
|
5-FU uses
|
CRC and other solid tumors, BCC (topical)
Synergy with methotrexate |
|
5-FU toxicity
|
1. Myelosuppresion which is NOT reversible with leucovorin
2. OD rescue with thymidine |
|
6-mercaptopurine (6-MP)
MOA and USES |
Purine analog --> dec de novo purine synthesis
Activated by HGPRTase USES = leukemias, lymphomas (not CLL or Hodgkins) |
|
6-MP TOX
|
bone marrow, GI, liver. Metabolized by xanthine oxidase, so inc toxicity with allopurinol
|
|
6-thioguanine (6-TG)
|
MOA = same as 6-MP. Purine analog that dec de novo synthesis of purines.
|
|
6-TG uses and toxicity
|
USES = ALL
TOX = bone marrow depression, liver Can be given with allopurinol |
|
Cytarabine MOA, USES and TOX
|
MOA = pyrimadine analog --> inhibits DNA polymerase
USES = AML, ALL, high grade NHL TOX = leukopenia, thrombocytopenia, megaloblastic anemia |
|
Antitumor antibiotics (4)
|
1. Dactinomycin
2. Doxorubicin 3. Bleomycin 4. Etoposide, teniposide |
|
Dactinomycin MOA, USES and TOX
|
MOA = intercalates DNA
USE = Childhood tumors (Wilm's, Ewings sarcoma, rhabdomyosarcoma) TOX = myelosuppresion |
|
Doxorubicin
|
MOA = generates free radicals. breaks DNA and inhibits replication
USE = Hodgkins lymphomas, also myelomas, sarcomas, and solid tumors of breast, ovary, lung. TOX = Alopecia, cardiotox, myelosuppression |
|
Bleomycin
|
MOA = induces free radical formation causing breaks in DNA strands
USES = testicular cancer, hodgkins TOX = pulm fibrosis, skin changes, minimal myelosuppression |
|
Etoposide
|
MOA = inhibits topoisomerase II leading to DNA degradation
USE = small cell carcinoma of the lung, prostate, testicular carcinoma TOX = Alopecia, myelosuppresion, GI irritation |
|
Alkylating agents
|
1. Cyclophosphamide, ifosfamide
2. Nitrosoureas 3. Busulfan |
|
Cyclophosphamide
Ifosfamide |
MOA = Covalently links DNA
USES = NHL, breast and ovarian carcinomas TOX = myelosuppresion, hemorrhagic cystitis. |
|
How can the toxicity of cyclophosphamide be prevented?
|
Admin of mesna.
|
|
Nitrosoureas
|
MOA = requires bioactivation, crosses the CNS
USES = brain tumors TOX = CNS toxicity (ataxia, dizziness) |
|
Busulfan
|
MOA = alkylates DNA
USE = CML and to ablate pt's bone marrow before bone marrow transplantation. TOX = pulm fibrosis, hyperpigmentation |
|
Microtubule inhibitors
|
1. Vincristine, vinblastine
2. Paclitaxol and the other --taxols |
|
Vincristine, vinblastine MOA
|
bind to tubulin in M-phase and block polymerization of microtubules so that mitotic spindles cannot form.
|
|
Vincristine TOX
|
neurotoxicity (areflexia, peripheral neuritis), paralytic ileus
|
|
Vinblastine TOX
|
VinBLASTine BLASTS bone marrow
|
|
Paclitaxel
|
Hyperstabalizes polymerized microtubules in M-phase so that mitotic spindle can't break down
USE = breast and ovarian carcinoma TOX = myelosuppression and hypersensitivity |
|
Breast cancer chemo drugs
|
Pactilaxel
Doxorubicin Cyclophosphamide Tamoxifen, raloxifene Trastuzumab (metastatic b cancer) |
|
Cisplatin
Carboplatin |
MOA = cross link DNA
USE = testicular, bladder, ovarian, and lung carcinomas TOX = nephrotoxicity and acoustic nerve damage |
|
Hydroxyurea
|
MOA = inhibits ribonucleotide reductase --> dec DNA synthesis (S phase specific)
USE = Sickle cell disease (inc HbF and reduces the rate of painful occlusive attacks) also CML and melanoma. TOX = bone marrow suppression, GI upset |
|
Prednisone
|
MOA = may trigger apoptosis
USE = most commonly used glucocorticoid in cancer chemo. Used in CLL, Hodgkins, autoimmune diseases TOX = cushing like syndrome, immunosuppression, cataracts, acne, osteoporosis, HTN, peptic ulcers, hyperglycemia, psychosis |
|
Tamoxifen
Raloxifene MOA and USE |
SERMS = receptor antagonists in breast and agonists in bone. Block the binding of estrogen to estrogen-R positive cells.
USE = breast cancer and to prevent osteoporosis |
|
Tamoxifen TOX
|
may inc risk of endometrial carcinoma via partial agonist effect. Hot flashes
|
|
Raloxifene TOX
|
Does not increase risk of endometrial carcinoma because it is an endometrial antagonist.
|
|
Trastuzumab (Herceptin)
MOA |
MOA = monoclonal AB against HER-2
Helps kill breast cancer cells that overexpress HER-2, possibly thru AB-dpnt cytotoxicity USE = metastatic breast cancer |
|
Imatinib
|
MOA = Philadelphia chromosome bcr-abl tyrosine kinase inhibitor
USE = CML, GI stromal tumors TOX = fluid retention |
|
Rituximab
|
MOA = monoclonal AB against CD20, which is found on most B-cell neoplasms
USE = NHL, RA (with methotrexate) |
|
MOPP regime used in Hodgkins
|
Mustargen
Oncovin Procarbazine Prednisone |
|
NSAIDS
|
reversible inhibition of COX (1 and 2)
blocks prostaglandin synthesis |
|
How do you close a PDA?
|
Indomethicin (an NSAID)
|
|
What's the difference between aspirin's MOA and other NSAID's MOA?
|
Aspirin = irreversible inhibition of COX
Other NSAIDS = reversible inhibition of COX |
|
Celecoxib
MOA |
COX-2 inhibitor. COX-2 is found in inflammatory cells and vascular endothelium and mediates inflam and pain. It's nice to not inhibit COX-1, because this maintains the gastric mucosa.
|
|
Celecoxib USE and TOX
|
USE = RA and OA, pts with gastritis or ulcers
TOX = inc risk of thrombosis. Sulfa allergy. Less toxic to GI mucosa |
|
Acetaminophen
|
MOA = reversibly inhibits COX, mostly in the CNS. Inactivated peripherally.
USE = no anti-inflamm effects TOX = hepatic necrosis, acetaminophen metabolites deplete glutathione and forms toxic tissue in liver |
|
Acetaminophen antidote
|
N-acetylcysteine regenerates glutathione
|
|
Bisphosphonates
|
"--dronate"
MOA = inhibit osteoclastic activity. reduce formation and resorption of hydroxyapatite USE = malignancy assoc hypercalcemia, Paget's disease of bone, postmenopausal osteoporosis TOX = Corrosive esophagitis (except zoledronate), nausea, diarrhea and osteonecrosis of jaw |
|
Why no salicylates in gout?
|
all but the highest doses will suppress uric acid clearance.
|
|
Probenecid
|
MOA = inhibits reabsorption of uric acid in the PCT (also inhibits the secretion of penicillin)
USE = chronic gout |
|
Colchicine
|
MOA = binds, stabalizes tubulin to inhibit polymerization, impairing leukocyte chemotaxis and degranulation.
USE = acute gout (along with NSAIDS, esp indomethicin, which is less toxic) |
|
TNF-alpha inhibitors (3)
|
1. Etanercept
2. Infliximab 3. Adalimumab |
|
Etanercept MOA
|
MOA = recombinant form of human TNF receptor that binds TNF
EtanerCEPT is a TNF decoy reCEPTor |
|
Etanercept USES
|
RA, psoriasis, ankylosing spondylitis
|
|
Infliximab
|
MOA = anti-TNF antibody
USES = Chron's disease, RA, ankylosing spondylitis TOX = predisposes to infxn (e.g. reactivation TB) |
|
Adalimumab
|
MOA = anti-TNF antibody
USES = RA, psoriasis, ankylosing spondylitis |
|
TNF-alpha definition
|
A cytokine involved in systemic inflamm. Primary role = regulating immune cells. Can be produced ectopically by malignancy and lead to secondary hypercalcemia.
|
|
H1 blockers
1st gen |
Diphenhydramine
Dimenhydrinate Chlorpheniramine |
|
H1 blockers
2nd gen |
Loratadine (Clariton)
Fexofenadine Desloratadine Cetirizine |
|
1st Gen H1 blockers
USES TOX |
USES = Allergies, motion sickness, sleep aid
TOX = sedation, antimuscarinic, anti-alpha-adrenergic |
|
2nd gen H1 blockers
USES TOX |
USES = Allergies
TOX = Much less sedating than 1st gen because of dec entry into CNS |
|
Non specific beta agonists
|
Isoproterenol
MOA relaxes bronchial smooth muscle (B2) USE asthma TOX tachy because it also blocks B1 |
|
B2 agonists
|
Albuterol
Salmeterol. |
|
Theophylline
|
USES = asthma
A type of methlxanthine drug. Limited use due to narrow TI. causes bronchodialation by inhibiting phosphodiesterase (cAMP --> AMP) and dec cAMP production |
|
Ipratropium
|
USES = asthma and COPD
competative block of muscarinic-R prevents bronchconstriction. |
|
Cromolyn
|
USE = asthma
prevents release of mediators from mast cells (prevents degranulation). Effective only for asthma prophylaxis, not an acute attack. Tox is rare |
|
Corticosteroids used to tx asthma:
Beclomethasone Prednisone |
1ST LINE FOR CHRONIC ASTHMA
inhibit the synthesis of all cytokines. Indirectly inhibits production of TNF-alpha. |
|
Zileuton
|
Antileukotriene
blocks conversion of arachidonic acid to leukotrienes. Leukotriene = bronchoconstriction |
|
Zafirlukast
Montelukast |
Antileukotrienes
Block leukotriene-R Good for aspirin-induced aspirin. |
|
Expectorants
|
Guifenesin: does not suppress cough reflex
N-acetylcysteine: mucolytic and can loosen mucous plugs in CF. Antidote for acetaminophen. |
|
Bosentan
|
USE = pulm HTN
decreases pulm vascular resistance by blocking enothelin-1-R |
|
Leuprolide
MOA USES |
GnRH analog
Pulsatile admin = agonist Continuous admin = antagonist USES = infertility (pulsatile), prostate cancer (continuous, use with flutamide), uterine fibroids |
|
Testosterone
USES TOX |
USES =
-Hypogonadism and promote dvlpmnt of secondary sex characteristics. -Stim of anabolism to promote recovery after burn/injury -Treat ER-positive breast cancer TOX = masculinization in females. Reduces intratesticular testosterone in males by inhibiting the release of LH = gonadal atrophy. inc LDL, dec HDL |
|
Finasteride (propecia)
|
5-alpha reductase inhibitor
(inhibit test --> DHT) Useful in BPH and promotes hair growth in male pattern baldness TOX = gynocomastia |
|
Flutamide
|
MOA = Nonsteroidal competative inhibitor of androgens at the testosterone-R.
USES = prostate carcinoma |
|
Ketoconazole and Spironolactone
|
Used to prevent hirsutism in PCOS. Both inhibit steroids
TOX = gynecomastia and amenorrhea |
|
Estrogens
|
USES = hypogonadism or ovarian failure, menstrual abnormalities, HRT in postmenopausals, used in men with androgen-dependant prostate cancer
TOX = inc risk of endometrial cancer, bleeding in postmenopausals, increased risk of thrombus CONTRA = ER-pos breast cancer, hx of DVT |
|
Tamoxifen
|
SERM
Antagonist on breast tissue, used to treat and precent recurrence of ER-positive breast cancer |
|
Clomiphene
|
SERM
Partial agonist at estrogen-R in hypothalamus. Inc release of LH and FSH from pituitary (abnormal feedback) stimulates ovulation. USES = infertility and PCOS TOX = hot flashes, ovarian enlargement, multiple preg |
|
Raloxiphene
|
SERM
Agonist on bone Reduces resorption of bone USES = osteoporosis |
|
HRT
|
Used for relief or prevention of menopausal sx (inc estrogen = dec osteoclast activity)
TOX = unopposed ERT inc risk of endometrial cancer so PROG is added. Possible CV risk |
|
Anastrozole/
Exemestane |
Aromatase inhibitors used in postmenopausals with breast cancer
|
|
Progestins
|
MOA = bind PROG-R, reduce growth and inc vascularization of endometrium
USES = OCPs treatment of endometrial cancer and abnormal uterine bleeding |
|
Mifepristone (Ru-486)
|
MOA = inhibitor of progestins at PROG-R
USES = termination of pregnancy. Admin'd with misoprostol (PGE1) TOX = heavy bleeding, GI effects, abd pain |
|
OCP MOA
|
Prevent estrogen surge so the LH surge never occurs = no ovulation
|
|
OCP cancer advantage
|
dec risk of endometrial and ovarian cancers
|
|
OCP disadvantages
|
Hypercoagulable state
Contraindicated in smokers >35yo |
|
Dinoprostone
|
PGE2 analog causing cervical dilation and uterine contraction, inducing labor
|
|
Ritodrine
Terbutaline |
B2-agonists that relax the uterus
Reduce premature contractions Prevent early delivery |
|
Tamsulosin
|
Alpha-1 blocker used to treat BPH by inhibiting smooth muscle contraction. Selective for the alpha-R on the prostate (alpha,1A,D) versus vascular (alpha1B)
|
|
Sildenafil
Vardenafil MOA and USES |
MOA = inhibit cGMP phosphodiesterase causing inc cGMP and smooth muscle relax in the corpus cavernosum --> inc blood flow and boner.
USES = ED |
|
Sildenafil
Vardenafil TOX |
HA, flushing, dyspepsia, IMPAIRED BLUE/GREEN VISION.
Risk of life threatening hypotension in pts taking nitrates. |
|
Glaucoma drugs
3 classes that dec aq humor |
alpha agonist
beta blocker diuretics all dec aqueous humor by diff MOA |
|
Epinephrine
|
Alpha-agonist
dec aq humor synthesis due to vasoC SE = mydriasis, stinging CONTRA = closed angle glaucoma |
|
Brimonidine
|
alpha agonist
dec aq humor synthesis |
|
Acetazolamide
|
CA inhibitor
inhibition of CA leads to dec aq humor secretion due to dec HCO3- |
|
Glaucoma drugs
2 classes that inc aq humor outflow |
Cholinomemetics
Prostaglandin |
|
Direct cholinomemetics
|
Pilocarpine
Carbachol |
|
Indirect cholinomemetics
|
Physostigmine
Echothiophate |
|
MOA of cholinomemetics in txmnt of glaucoma
|
inc outflow of aq humor
contract ciliary muscle and open trabecular meshwork into canal of Schlemm |
|
DOC in emergency closed angle glaucoma
|
PILOCARPINE
|
|
Prostaglandin txmnt in glaucoma
|
Latanoprost
MOA = inc outflow of aq humor SE = darkens color of iris |
|
Opioid analgesics
(list of drugs) |
Morphine
Fentanyl Codeine Heroin Methadone Meperidine Dextromethorphan |
|
Opioids MOA
|
Agonists at opioid-R (mu, delta, kappa) to modulate synaptic transmission = open K+ channels, close Ca++ channels --> dec synaptic transmission.
Inhibit the release of ACh, NE, 5-HT, glutamate and substance P |
|
Opioids USE
|
Pain, cough suppression (dextromethorphan), diarrhea (loperamide and diphenoxylate), acute pulm edema, maintenance program for addicts
|
|
Opioids TOX
|
Addiction
Respiratory depression Constipation Miosis (PINPOINT) Txmnt = naloxone or naltrexone (opioid-R blocker) |
|
Butorphanol
|
MOA = paritial agonist at opioid-mu-R, agonist at kappa
USE = pain TOX = less resp depression than regular opioids. causes withdrawal if pt is on full opioid agonist |
|
Tramadol
|
MOA = weak opioid agonist, also inhibits 5-HT and NE reuptake
USE = chronic pain TOX = similar to opioids. dec seizure threshold |
|
Carbemazepine
|
TCA
1st line = tonic-clonic and trigem neuralgia TOX = liver, SIADH, aplastic anemia MOA = inc Na+ channel inactivation |
|
Phenytoin
|
1st line = tonic clonic, prophy for status epilepticus
IV route = fosphenytoin MOA = inc Na+ channel inactivation |
|
Lamotrigine
|
MOA = blocks voltage gated Na+ channels
USED = partial, tonic clonic |
|
Topiramate
|
MOA = blocks Na+ channels, inc GABA action
|
|
Phenobarbital
|
1st line = pregnant women, kids
MOA = inc GABAa action |
|
Valproic acid
|
1st line = tonic clonic
MOA = inc Na+ channel inactivation, inc GABA concentration Also used for myoclonic seizures |
|
Ethosuximide
|
1st line = absence seizures
MOA = blocks thymic T-type Ca++ channels |
|
Benzo's:
Diazepam Lorazepam |
1st line = acute status epi
MOA = inc GABAa action Also used for seizures of eclampsia |
|
Seizures of eclampsia DOC
|
Magnesium sulfate
|
|
What are the three 1st line drugs for tonic-clonic?
|
1. Phenytoin
2. Carbamazepine 3. Valproic acid |
|
Benzo TOX
|
Sedation, tolerance, dependence
|
|
Carbamazepine TOX
|
Agranulocytosis (most feared)
P450 inducer Steven Johnsons Diplopia Ataxia liver tox teratogenesis |
|
Ethosuximide TOX
|
Steven Johnson
GI distress, urticaria, fatigue, HA |
|
Phenobarbitol TOX
|
Sedation, tolerance, dependance, INDUCE p450
|
|
Phenytoin TOX
|
Teratogenesis (fetal hydantoin syn)
Gingival hyperplasia SLE-like syndrome hirsutism, ataxia, nystagmus, sedation, megaloblastic anemia |
|
Valproic acid TOX
|
Rare but fatal liver tox (moniter LFT)
Neural tube defects in fetus tremor, weight gain CONTRA in preggos |
|
Lamotrigine TOX
|
Steven Johnsons
|
|
Topiramate TOX
|
Sedation, mental dulling, kidney stones, weight loss
|
|
Barbiturates
(list) |
Phenobarbital
Pentobarbital Thiopental Secobarbital |
|
Barbiturates MOA and USE
|
Facilitate GABAa action by inc DURATION of Cl- channel opening and thus dec firing
USE = sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental) |
|
Barbiturates TOX...again
|
Dependence
P450 INDUCTION additive effects with other CNS depressants (EtOH) Resp or CV depression Tx OD symptomatically (resp support, inc BP) |
|
Benzos (list)
|
Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, alprazolam and chlordiazepoxide
|
|
DOC for acute EtOH withdrawal
|
Chlordiazepozide (a benzo, silly!)
|
|
Benzo's MOA
|
Facilitate GABAa action by inc FREQUENCY of Cl- channel opening.
dec REM sleep |
|
Benzo's versus Barb's and their MOA on the Cl- channel
|
Benzo = inc FREQ of opening
Barbs = inc DURATION of opening |
|
Benzo OD txmnt
|
Flumazenil (competitive antagonist at GABA benzo receptor)
|
|
What are the short acting benzo's and what are you at inc risk for when using them?
|
Triazolam
Oxazepam Midazolam These have the highest abuse potential |
|
Nonbenzo hypnotics (list)
|
Zolpidem (Ambien)
Zaleplon Eszopiclone |
|
Nonbenzo hypnotics
MOA USE TOX |
MOA = Act via the BZI-R subtype and is revered by flumazenil
USE = insomnia TOX = ataxia, HA, confusion. Less day-after psychomotor depression and few amnestic effects. Lower dependence risk than benzos |
|
low solubility in blood =
|
rapid induction and recovery times
high solubility in blood will require more drug to saturate blood = slower onset of axn |
|
increase solubility in lipids =
|
inc potency (1/MAC)
|
|
Inc MAC = ___ potency
|
inc MAC = dec potency
|
|
Inhaled anesthetics (list)
|
Halothane
Enflurane Isoflurane Sevoflurane Methoxyflurane NO |
|
Inhaled anesthetics
MOA EFFECTS TOX |
MOA = unknown
EFFECTS = myocardial and resp depression, n/v, inc cerebral blood flow (but dec cerebral demand) TOX = malignant hyperthermia |
|
Halothane TOX
|
Hapatotoxicity
|
|
Methoxyflurane TOX
|
nephrotoxicity
|
|
Enflurane TOX
|
Proconvulsant
|
|
Nitrous oxide TOX
|
expansion of trapped gas
|
|
IV anesthetic classes
|
Barbs
Benzos Ketamine (arylcyclohexylamine) Opiates Propofol |
|
Thiopental
|
Barbiturate
Used for induction of anesthesia and short surgical procedures High potency, high lipid solubility, rapid CNS entry dec cerebral blood flow |
|
Midazolam
|
Benzo
Most common drug used for endoscopy Can cause severe post-op resp depression, dec BP (tx OD with flumazenil) |
|
Ketamine
|
PCP analog that act as dissociative anesthetics
MOA = block NMDA-R Cardio stimulants Cause disorientation, hallucination, and bad dreams inc cerebral blood flow |
|
Opiates
|
Morphine, fentynyl
Used with other CNS depressants during general anesthesia |
|
Propofol
|
Used for rapid anesthesia induction and short procedures.
Less post-op nausea than thiopental Potentiates GABAa |
|
Local anesthetics (list)
|
Esters = procaine, cocaine, tetracaine
Amides have 2 I's= lidocaine, mepivacaine, bupivacaine |
|
Locals MOA
|
Block Na+ channels
Preferentially bind activated Na+ channels, so most effective in rapidly firing neurons |
|
Order of blockade with locals
|
small myelinated > small unmyelin > large myelinated > large unmyelin
|
|
In infected tissue, you will need more local anesthetic. Why?
|
Infected tissue = acidic tissue
alkaline anesthetics won't be able to penetrate the tissue effectively, so you will need more |
|
Why are locals usually given with EPI?
|
EPI = vasoC and it will enhance the local action (dec bleeding, inc anesthsia and dec systemic concentration)
|
|
Cocaine TOX
|
Arrythmias
|
|
Dantrolene
|
DOC for malignant hyperthermia
Also used for treatment of neuroleptic malignant syndrome (toxicity seen with neuroleptics) |
|
Neuromuscular blocking drugs
USES |
muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs autonomic) nicotinic receptor
|
|
Succinylcholine
|
depolarizing neuromuscular blocker
TOX = hyperCa++ and hyperK+ |
|
Nondepolarizing neuromuscular blockers
|
Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium
|
|
DA-R agonists
|
Bromocriptine, Pramipexole, Ropinirole
(Bro, ro, apo, pram) |
|
What drug is used to increase DA and also as an antiviral against influenza A and rubella?
|
Amantadine
TOX = ataxia |
|
L-dopa/carbidopa
|
L-dopa = Converted to DA in the CNS
Carbidopa = peripheral decarboxylase inhibitor, dec amount of DA in periphery (because you want it in the brain) |
|
L-dopa/carbidopa TOX
|
arrythmias from peripheral conversion to DA.
Long term use can lead to dyskinesia following admin, akinesia between doses |
|
Selegiline
MOA USE TOX |
MOA = selectively inhibits MAO-B.
MAO-B metabolizes DA over NE and 5-HT, so inhibiting MAO-B with inc DA USE = adjunctive therapy to L-dopa in PD TOX = enhance adverse effects of L-dopa |
|
Entacapone
Tolcapone |
COMT inhibitors
Prevent L-dopa degradation and thus inc DA availability to CNS |
|
What drug is used to curb excess ACh activity in PD?
|
Benztropine
Antimuscarinic Improves tremor and rigidity, little effect of bradykinesia |
|
Memantadine
MOA USE |
MOA = NMDA-R antagonist
helps prevent excitotoxicity USE = Alz. Disease |
|
Donepezil
Galantamine Rivastigmine MOA USE |
MOA = AChE inhibitors
USE = Alz. Disease |
|
What NT imbalances are seen in Huntington's disease?
|
inc DA
dec GABA and ACh |
|
What drugs are used to tx Huntingtons?
|
Reserpine and tetrabenazine = amine depleating
Haloperidol = DA-R antagonist |
|
Sumatriptan
MOA USE TOX |
MOA = 5-HT1b/1d agonist
causes vasoC, inhibition of trigeminal activation and inhibits vasoactive peptide release USE = migraines, cluster attacks TOX = coronary vasospasm CONTRA = pts with CAD |
|
Mannitol
MOA |
MOA = osmotic diuretic, inc tubular fluid osmolarity producing inc urine flow
SOA (site of axn) = PCT |
|
Mannitol
USES |
Shock, drug OD, inc IOP or ICP
|
|
Mannitol
TOX |
Pulmonary edema, dehydration.
CONTRA = anuria, CHF |
|
Acetazolamide
MOA |
CA inhibitor
Causes self-limited NaHCO3 diuresis and reduction in total-body HCO3- stores. SOA = PCT |
|
Acetazolamide
USE |
Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness
ACIDazolamide causes ACIDosis |
|
Acetazolamide
TOX |
Hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy
|
|
Furosemide
MOA |
Sulfonamide loop diuretic
Inhibits cotransport system (Na+, K+, 2Cl-) of thick ascending LOH. abolishes hypertonicity of medulla, preventing concentration of urine...inc Ca++ excretion (loops lose Ca++) SOA = LOH, esp thick ascending loop |
|
Furosemide
USE |
Edematous states (CHF, cirrhosis, nephrotic syndrome, pulm edema), HTN, hyperCa++ (because LOOPs LOSE Ca++)
|
|
Furosemide
TOX |
Ototoxicity, HypoK+, dehydration, allergy (sulfa), nephritis, gout
|
|
What can you use for diuresis in pt's allergic to sulfa drugs?`
|
Ethacrynic acid
Can also be used in gout, hyperurecemia (unlike furosemide) |
|
Hydrocholothiazide
MOA |
Thiazide diuretic
Inhibits NaCl reabsorption in early DCT, reducing the diluting capacity of nephron. dec Ca++ excretion SOA = DCT |
|
Hydrocholothiazide
USE |
HTN, CHF, idiopathic hypercalcuria, nephrogenic DI
|
|
Hydrocholothiazide
TOX |
HypoK+ metabolic acidosis
HypoNa+ Hyperglycemia Hyperlipidemia Hyperuricemia Hypercalemia Sulfa allergies |
|
K+ sparing diuretics (list)
|
Spironolactone
Triamterene Amiloride Eplerenone |
|
K+ sparing diuretics
MOA |
Spironolactone = comp aldosterone-R antagonist in the cortical collecting tubule.
Triamterene/Amiloride = block Na+ channels in the CCT |
|
K+ sparing diuretics
USES |
Hyperaldosteronism
K+ depletion CHF |
|
K+ sparing diuretics
TOX |
HyperK+ (arrythmias)
Spironolactone has endocrine effects due to aldosterone antagonism (gynocomastia, antiangrogenic effects) |
|
ACE-I
list MOA |
Captopril, enalapril, lisinopril
MOA = inhibit ACE, reducing levels of AT-II and preventing inactivation of bradykinin (a vasoD) NOTE: renin is inc (loss of neg feedback) |
|
ACE-I
USES |
HTN, CHF, diabetic renal disease
|
|
When are ACE-I contraindicated?
2 situations |
1. Preggos
2. bilateral renal artery stenosis, ACE-I dec GFR by preventing constriction of efferent arterioles |
|
ACE-I
TOX |
Cough, cough, cough
Angioedema Proteinuria Taste changes hypOtension Pregnancy problemos Rash Inc renin Lower AT-II CAPTOPRIL also hyperk+ |
|
Effect of diuretics on urine NaCl
|
All diuretics inc urine NaCl
(serum NaCl may dec) |
|
Effect of diuretics on urine K+
|
All diuretics (except K+ sparing) inc urine K+
So serum K+ may dec |
|
What diuretics cause acidemia?
|
CA inhibitors (acetazolamide)
K+ sparing |
|
What diuretics cause alkalemia?
|
Loops
Thiazides |
|
What diuretics cause inc urinary Ca++?
|
Loops
HypoCa++ and inc urine Ca++ |
|
What diuretics cause dec urinary Ca++?
|
Thiazides
hyperCa++ and dec urine Ca++ |
|
Delerium tremens txmnt
|
Benzos
(chlordiazepoxide) |
|
Wernicke's encephalopathy
(as in Wernicke Korsakoff) |
Triad:
confusion opthalmoplegia ataxia |
|
Korsakoff's psychosis
(as in Wernicke Korsakoff) |
Irreversible memory loss
Confabulation Personality change |
|
Txmnt of W.K syndrome
|
IV thiamine
|
|
CNS stimulants (list)
|
Methylphenidate
Dextroamphetamine Mixed amphetamine salts |
|
CNS stimulants
MOA USES |
MOA = inc catecholamines at the synaptic cleft
USE = ADHD, appetite control, narcolepsy |
|
Typical Neuroleptics
|
Haloperidol + "--azines"
Trifluoperazine Fluphenazine Thioridazine Chlorpromazine |
|
Typical Neuroleptics
MOA |
All typicals block DA D2-R (inc cAMP concentration)
|
|
Typical Neuroleptics
USE |
Schizophrenia (tx primarily positive sx)
Psychosis Acute mania Tourette's |
|
Typical Neuroleptics
Neuroleptic malignant syndrome (clinical picture and txmnt) |
Rigidity, myoglobinuria, autonomic instability, hyperpyrexia.
TX = Dantrolene (muscle relaxant) DA agonists (like bromocriptine) |
|
High potency typical neuroleptics and assoc SE
|
Haloperidol, trifluoperazine, fluphenazine
SE = neurologic (EPS) |
|
Low potency typical neuroleptics and assoc SE
|
Thioridazine, chlorpromazine
SE = non-neurological (anticholinergic, antihistamine, and alpha blockade) |
|
Chlorpromazine SE
|
Corneal deposits
|
|
Thioridazine SE
|
reTinal deposits
|
|
Evolution of EPS
|
4 hours dystonia
4 days akinesia 4 weeks akatheisa (restlessness) 4 months tardive dyskinesia |
|
Atypical neuroleptics
(list) |
Olanzapine, clozapine, quetipine, risperidone, aripiprazole, ziprasidone
|
|
Atypical neuroleptics
MOA |
Block receptors:
5-HT2 DA alpha H1 |
|
Atypical neuroleptics
USE |
Schizophrenia (tx's both positive and negative sx)
Olanzapine = OCD, anxiety disorder, depression, mania, Tourette's |
|
Atypical neuroleptics
TOX |
fewer EPS and anticholinergic SE than typicals.
Olanzapine and clozapine can cause significant weight gain. Clozapine = granulocytosis |
|
Lithium MOA
|
Unknown
Possibly inhibition of phosphoinositol pathway |
|
Lithium
USE |
Mood stabalizer for bipolar disorder
Blocks relapse and acute mania events. SIADH |
|
Lithium TOX
|
Narrow TI requires close monitering
Movement (tremor) Nephrogenic DI (ADH antagonism, polyuria) HypOthyroidism Pregnancy problems (Epstein anomaly, malformation of great vessels) |
|
Lithium excretion
|
Almost exclusively excreted by kidneys. Most is reabsorbed in PCT following Na+ reabsorption.
|
|
Buspirone
MOA USE |
MOA = stimulates 5-HT1A receptors
USE = Generalized anxiety disorder. Does not cause sedation, addiction or tolerance. Does not interact with EtOH (versus benzo's and barbs) |
|
TCAs
|
Imipramine
Amitryptyline Desipramine Nortriptyline Clomipramine Doxepin Amoxapine |
|
TCA
MOA and USE |
MOA = Block reuptake of NE and 5-HT
USE = Major depression Bedwetting (imipramine) OCD (clomipramine) Fibromyalgia |
|
TCA
SE |
Sedation, alpha-blocking effects, atropine like (anticholinergic) stuff like tachy, urinary retention.
Desipramine is least sedating and has lower seizure threshold tertiary TCAs (amitriptyline) have more antichol effects than secondary TCAs (nortriptyline) |
|
TCA
TOXICITY |
Tri-C's =
Convulsions Coma Cardiotoxicity (arrythmias) also resp depression, hyperpyrexia Use nortriptyline in the elderly because they can dvlp confusion and hallucinations due to antichol effects. |
|
SSRI
|
Fluoxetine
Paroxetine Sertraline Citalopram |
|
SSRI MOA and USE
|
MOA = serotonin-specific reuptake inhibitors
USE = Depression, OCD, bulimia, social phobias |
|
High potency typical neuroleptics and assoc SE
|
Haloperidol, trifluoperazine, fluphenazine
SE = neurologic (EPS) |
|
Low potency typical neuroleptics and assoc SE
|
Thioridazine, chlorpromazine
SE = non-neurological (anticholinergic, antihistamine, and alpha blockade) |
|
Chlorpromazine SE
|
Corneal deposits
|
|
Thioridazine SE
|
reTinal deposits
|
|
Evolution of EPS
|
4 hours dystonia
4 days akinesia 4 weeks akatheisa (restlessness) 4 months tardive dyskinesia |
|
Atypical neuroleptics
(list) |
Olanzapine, clozapine, quetipine, risperidone, aripiprazole, ziprasidone
|
|
Atypical neuroleptics
MOA |
Block receptors:
5-HT2 DA alpha H1 |
|
Atypical neuroleptics
USE |
Schizophrenia (tx's both positive and negative sx)
Olanzapine = OCD, anxiety disorder, depression, mania, Tourette's |
|
Atypical neuroleptics
TOX |
fewer EPS and anticholinergic SE than typicals.
Olanzapine and clozapine can cause significant weight gain. Clozapine = granulocytosis |
|
Lithium MOA
|
Unknown
Possibly inhibition of phosphoinositol pathway |
|
Buspirone
MOA and USE |
MOA = stimulates 5-HT1a receptors
USE = GAD. Does not cause sedation, addiction, tolerance. Does not interact with EtOH. |
|
TCAs
|
Imipramine, amitriptyline, desipramine, nortriptyline, clomipramine, doxepin, amoxapineq
|
|
TCA MOA
|
Block reuptake of NE and 5-HT
|
|
TCA USES
|
Major depression
Bedwetting (imipramine) OCD (clomipramine) Fibromyalgia |
|
TCA
SE |
Sedation, alpha blocking effects, atropine-like (anticholergic) effects like tachy, urinary retention.
tertiary amines (amitriptyline) have more anticholinergic effects than secondary amines (nortriptyline) |
|
TCA
TOX |
Tri C:
Convulsions Coma Cardiotoxicity (arrythmias) also resp depression, hyperpyrexia. confusion and hallucinations in the elderly due to antichol effects (use nortriptyline) |
|
How do you tx TCA toxicity?
|
NaHCO3 for cardiotox
|
|
SSRI
|
Fluoxetine
Paroxetine Sertraline Citalopram |
|
SSRI
MOA and USES |
MOA = serotonin-specific reuptake inhibitors
USE = depression, OCD, bulimia, social phobias |
|
SSRI
tox |
GI distress, anorgasmia
Less SE than TCAs |
|
Serotonin syndrome
What is it? What is the presentation? How to tx it? |
An adverse effect of SSRI's when they're taken with another drug that increases 5-HT (like MAO-I)
Presents with hyperthermia, muscle rigidity, cardiovascular collapse, flushing, diarrhea, seizures. tx with cyproheptadine (5-HT2 receptor antagonist) |
|
SNRI's
|
Venlafaxine
Duloxetine |
|
SNRI
MOA |
Inhibit serotonin and NE reuptake
|
|
SNRI
USES |
Depression
Venlafaxine is also used in GAD Duloxetine is also used for diabetic peripheral neuropathy Duloxetine has a greater effect on NE |
|
SNRI
tox |
inc BP most common
|
|
MAO-Inhibitors
|
Phenelzine
Tranylcypromine Isocarboxazid Selegiline (selective MAO-B inhibitor) |
|
MAO-I
MOA and USE |
Nonselective MAO inhibition increases levels of amine NT (NE, 5-HT, DA)
USE = atypical depression, anxiety, hypochondriasis |
|
MAO-I
tox |
Hypertensive crisis with tyramine ingestion (wine and cheese) and beta agonists. CNS stimulation
CONTRA = with SSRI's or meperidine |
|
Bupropion
|
inc NE and DA via unknown MOA
USES = smoking cessation and depression TOX = stimulant SE (tachy, insomnia), HA, seizure in bulimic pts. No sexual effects |
|
Mirtazepine
|
alpha-2 blocker.
Inc release NE and 5-HT and potent 5-HT2 and 5-HT3 receptor blocker. TOX = sedation, inc appetite, weight gain, dry mouth |
|
Maprotiline
|
Blocks NE reuptake
TOX = sedation, orthostatic hypotension |
|
Trazodone
|
Primarily inhibits 5-HT reuptake.
Used for insomnia (high doses are needed for antidepressant effects). TOX = sedation, nausea, priapism, postural hypotension |
|
DOC for depression with insomnia
|
Mirtazepine
|
|
DOC for Tourette's
|
Haloperidol
|