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*SAM- S Adenosine Methionine

*Carnitine- Transports Fatty acids in to the mitochondria for Beta-oxidation to acetyl


- Impaired in Alcoholism.

*Amanita Toxin - Binds to DNA dependent RNA Polymerase II, halts mRNA synthesis.

- Accumulates in rapidly dividing cells, thus cause more damage to these

cells / organs. (eg. hepatocytes, Intestinal cells, renal cells).

*Ricin (from castor oil) - Halts Protein Synthesis.

*STOP CODON - Codes for Releasing Factor 1.

*Colchicine - Impairs Neutrophil migration and phagocytosis by interfering with

microtubule formation.

- Decreases tyrosin kinase activity thus decreased Neutrophil activation.

*Osteopetrosis - Increased bone thickness and density

d/t- Impaired osteoclast activity

*anti-CCP antibody - RA Specific.

*RF - Antibodies against Fc portions of IgG. Found inRA, but non-specific.

*anti-Centromere antibody - CREST Syndrome

*anti-dsDNA - SLE.

*anti-Phospholipid antibodies - SLE & Antiphospholipid antibody syndrome.

*Glycine - M/C (every third) amino acid in collagen fibers. D/t its smallest size, it
gets fit into the restricted space of triple helix.

*Proline - essential for alpha helix in collagen fibers, as it's ring structure produces a
bend into polypeptide chains.

*Ketogenic Amino acids - Leucine and lysine

*Pyruvate Carboxylase - converts Pyruvate to OAA, requires Biotin

*Enhancer region - can be located anywhere upstream/ downstream/ within the

introns or may be thousands of bases away from the gene.
*Promotor - 25 Bases (TATA/Hogness box) or 70 bases (CAAT Box) upstream of the
gene. These are the sites for attachment of Polymerase II.

*Coenzymes required for Pyruvate Dehydrogenase (PDH) and Ketoglutarate

Dehydrogenase - thymine, lipoic acid, Fad, Nad, CoA( Active form of Pentothenic

*CoA - Pentothenic acid to CoA - ATP dependent phosphorylation

- In SYnthesis of Vit A, D, Cholesterol, Steroids, Heme A, Fatty Acids, Amino Acids

and Proteins.

*Citrullinemia - Urea cycle disorder,

- d/t deficiency of Arginosuccinate synthatse (ATP is a cofactor)

*Methylmalonic acidemia Deficiency of Methylmalonate Mutase ( Vit. B12)

*Homocystinuria - Premature Atherosclerosis (MI in very young), Def. of

cystathionine synthase.

*Homocysteine to cysteine - Cystathionin synthase & Cystathionase(B6 Required)

*Homocysteine to Methionine - Folate & Vit. B12 dependent process.

*Ketone Body Utilizing parts- Skeletal Muscles, Cardiac muscles, Renal Cortex, Brain.

*Ketone bodies cant be utilized by - RBCs ( no Mitochondira, so no use of

acetoacetate), Liver Cells (lacks Succinyl CoA-Acetoacetate CoA Transferase
(thiophorase) which is required to convert acetoacetate to acetoacetyle CoA)

*Guanosine capping- 5' 7-methyl guanosine

*Poly A tail - at 3' end. Gene has consensus sequence (AAUAAA) at 3' end, after
which poly A tail is added.

- it protects mRNA in cytoplasm from degradation.

*Introns - Non-coding sequences in mRNA (Intruders).

*Propionyl CoA - produced by Valine, Isoleusine, Methionine, Threonin, odd

numbered Fatty acids and cholesterol side chain.

*Lead - Inhibits d-amino levulinate Dehydratase & Ferrochelatase

*Tetrahydrobiopterin - cofactor in the synthesis of Tyrosine, dopa, serotonin & Nitric

*Maple syrup urine - Defective oxidative decarboxylation of branched chain amino
acids ( leucine, isoleucine, Valine) by branched chain a-ketoacid dehydrogenase

*Homocystienuria - Methionin restriction and cystiene supplementation is T/t.

*Branched chain a- ketoacid dehydrogenase, Pyruvate dehydrogenase & a-

ketoglutarate dehydrogenase require 5 cofactors - Thiamiane pyrophosphate,
Lipoate, CoA, FAD, NAd( Tender Loving Care For Nancy).

*Only Vit. B12 & folate are reserved in Liver in sufficient amount to last for YEARS.
Other Vit. (Viz. A,E,K) last only for few months.

*Vit. K Stores last 1-3 Weeks only.

*Heme -> -ve Feedback on d-ala Synthatase.

*HbF- Replaced by HbA in 6 months.

*UDP Glucuronyl Transferase - -nt in Criggler-Najjar, Low in Gilbert & Infants.

- unconjugated jaundice.

*Defective secretion of Conjugated Bilirubin - Rotor Syndrome, Dubin Johnson Syn.

*Tumor lysis syndrome - large quantity of Uric acid is produced which can cause
Acute Renal Failure.

*Rasburicase - Recombinant Urate Oxidase. Converts uric acid to allantoin which is

5-10 times more water soluble than urate. given for tumor lysis syndrome.

*Imperforate Anus - A/w GUT malformations.

*Infantile hydrocele is equivalent to adult Indirect Hernia. (Hydrocoele n Indirect

hernia are formed through the same mechanism through tubovaginalis (?))

*Late division of Monozygotic twins results in 1 amniotic sac and 1 chorionic sac.

*Sertoli cells will inhibit the involution of Mullerian (paramesonephric) ducts. Thus
inhibiting the development of internal female genitalia.

*Leydig cells produce testosterone, thus developing wullfian duct and male external

*Leydig cells produce Testosterone, which gives negative feedback to LH.

*Sertoli cells produce Inhibin b, which gives negative feedback to FSH.

*The hormones that regulate the synthesis of surfactantinclude are - Glucocoticodes

( Max Effect), prolactin, insulin, estrogen, androgen, thyroid and catecholamines.
*Neural Crest Cells- Form Submucosal (Meisner's) and Myenteric (Auerbech"s) Plexi.

*hCG - Glycoprotein Hormone Produced by the placenta, which resembles LH, FSH &

- THE MAIN function of hCG is to support Corpus Lutium, to produce progesterone.

*Triple Test - afp, hcg & estriol levels. B/w 16-18 weeks.

- If triple test is abnorml, then usg. If usg is consistent with pregnancy dates
n there r no anatomic abnormalities, then Amniocentesis.

*True Diverticulum - Meckle's Diverticulum, Normal Appendix

*Pseudo-diverticulum - Zenker's Diverticulum, Commomn Colon Ticks

*Mackel's Diverticulum - Remnant of Omphalomesentric (vitelline) duct.

Connected to Ileum, 2 feet from iliocoecal valve.

M/c ectopic Mucosa - Gastric Mucosa F/B Pancreatic tissue.

*Freckles - Ephelides

*M/C congenital anomaly - Accessory nipples.

*Ureteric Bud Derivatives - Collecting system of kidney, including collecting tubules

& ducts, Major and minor callyces, Renal Pelvis and Ureter.

*Metanephric Blastema derivatives - Glomeruli, Bowman's Space, Proximal Tubule,

Loop of henle And Distal Collecting tubules.

*Alpha Fetoproteins (AFP) and Acetylcholinestrase - Neural Tube Defects

*The secondary Oocytes remain frozen until fertilization occurs in Fallopian tube.

*Dorsal Pancreatic Bud - Forms Tail, body and most of head of pancreas along with
dorsal (accessory) Pancreatic duct of Santorini.

*Vetral Pancreatic Bud - Uncinate process, Inferior/posterior portion of head and

major pancreatic duct (of wirsung).

- Both, Ventral and dorsal buds are derived from the duodenal portion of the
*Vit. A overdose in pregnancy - Craniofacial Deformity, Posterior fossa CNS Defects,
Auditory defects and abnormalities of great vessels. (similar to DiGeorge

*Cleft Lip - d/t non-fusion of Maxillary prominence with intermaxillary Segment.

*Cleft Palate - Non-fusion of Palatine shelves growing from maxillary prominences

with one another n intermaxillary segment (primary Palate).

*Melanoma - Commonly migrates to Brain, Intestine, bone, liver and Lungs.

- Malignancy of Melanocytes, which are derived from Neural crest cells.

*Kallman's Syndrome - Failure of migration of GnRH secreting neurons from

Olfactory lobe to Hypothalamus.

*Apple Peel Atresia - Atresia of small intestine in neonate d/t SMA obstruction.

- This menifests as a blind-ending proximal jejunum with absence of a long

length of small bowell and dorsal mysentery. The terminal ileum distal to atresia
assumes a spiral configuration around an ileocolic vessel.

*Polyhydramnios causes -

1. Decreased Fetal Swallowing ( GIT Obstruction eg. Duodenal,

Esophageal, Intestinal atresia) or anencephaly.

2. Increased fetal Urination [High Cardiac Output (eg. Anemia)] or twin

to twin transfusion syndrome.

*Vancomycin induced RED MAN Syndrome - Mediated by Histamin

*Substance P - 11-amino acid polypeptide. pain neurotransmitter in both peripheral

and central nervous system.

- Capsaicin - reduces pain by decreasing it's level in Peripheral nervous


- in CNS, It's also thought to regulate mood, anxiety, and stress behavior.

*Niacin - Causes flushing mediated by Prostaglandin. T/t- Aspirin

- Antihyperlipidimic action- Decreases Cholesterol-> VLDL, VLDL->LDL.

- It also increases HDL by 25-30%.

- Potentiates the effect of some Antihypertensive meds d/t its vasodilatory


- increases Insulin resistance. Worsens DM.

*Segmental Glomerulosclerosis - Heroin and pamidronate

*Membranous Glomerulopathy - Gold

*Tubular Necrosis - Aminoglycosides, Foscarnet, Radio Contrast, amphotericin B and


*Drug induced tubular obstruction - Sulfonamides, Methotrexate, I/V Acyclovir and


*Acute Interstitial infiltration - Methicillin (M/C), NSAIDs, Acetazolamide, allopurinol,

Cisplatin and Sulfonamides.

*Chronic Interstitial Nephritis - Li, Cyclosporin.

*ACEI - cause decrease in GFR by reducing efferent arteriole vasoconstriction, thus

increasing Serum Creat. by 30% in 2-5 days.

*Nitropruside - Antihypertensive with mixed arterial and venous vasodilatory


ADR - Nitropruside ->Cynide. accumulation of cynide causes poisoning.

Cyanide via liver rhodanase-> thiosynate.

Antidote - Sodium thiosulfate. it gives additional Sulfur to liver rhodanase to

enhance metabolism and detoxification of cyanide to thiocyanate.

*Fenoldopam - Benzapine derivative of Dpamine, which has selective effect on D1


- Indicated in hypertensive emergencies only.

MOA - 1.) D1 receptor activation -> activayes adenylyl cyclase ->raises cyclic
AMP -> Arterial dilatation (espacially Renal, Coronary and mesenteric) -> decreases

2.) D1 receptor in kedneys increses water and Sodium excretion.

- Only I/v drug that improves renal perfusion, so beneficial in renal


*During continuous infusion of a drug metabolized by first order kinetics, the steady
state concentration is reached in 4-5 lives.

*Dopamine -

1.) Low dose - Stimulate D1 receptor in renal and mesenteric vessels->

vasodilation and increased blood flow at these sites.
2.) Higher doses - Stimulation of cardiac beta-1 receptor-> increased cardiac

3.) still higher doses - generalised vasoconstriction by alpha-1 adrenergic


*Nor-epinephrine - I/v may cause Indurations and pallor of the surrounding tissue,
D/t extravasation of NE-> intense alpha1 mediated vasoconstriction which can lead
to local tissue necrosis.

T/t- infiltration of affected area with 5-10 mg of phentolamine mesylate(alpha

receptor blocker) in 10-15 cc NaCl, with-in 12 hours of extravasation.

*Isoproterenol - beta-2 agonist, acts particularly in striated muscles, renal and

mesenteric vascular beds.

*Enzyme Inducers:- Carbamazepine, Phenobarbitol, phenytoin, rifampin,

Griseofulvin, nevirapine, Chr. ALchohol abuse, St. Johns wart.

*Enzyme Inhibitor:- Cimetidine, Ciprofloxacin, Macrolide(except Azithromycin), Azole

antifungals, Grapefruit juice, Isoniazid, Ritonavir(PI), Quinidine.

*Statins - lower LDL

*Fibrates - lower Triglycerides

*Niacin - increases HDL (ADR - Increase Uric acid Level)

*STATINS have smaller but significant effect in lowering triglycerides. So used in

mild-moderate hyperlipidemia.

*Statins reduce serum cholesterol concentration by inhibiting HMG CoA reductase,

thus causing an increase in LDL Receptors on hepatocytes, which reduces serum
LDL concentration.

*Statins are metabolized in the liver (except Pravastatin) by Cyt3A4. So, enzyme
inhibitors will increase their Concentration and enzyme inducers will decrease their

-ADR- Heptitis and Myopathy. Myopathy is maximally caused by simvastatin.

When given with Fibrates, its dosage must not exceed 10mg.

*Fibrates cause myopathy by:-

1. Gemfibrozil- Increases the concentration of statins.

2. Fenofibrates- Causes myopathy itself.

*Use of medications to raise HDL doesn't improve cardiovascular outcomes.

*Pharmacological treatment of patients with low HDL levels should focus on
lowering LDL cholesterol with Statins, as these are the most effective lipid lowering
drugs for preventing cardiovascular events.

*HDL - in reverse cholesterol transport i.e. transport of cholesterol from peripheral

tissues to liver.

1.)- Direct pathway- HDL delivers cholesterol ester to hepatocytes by

scavenger receptors (SCARB1) on hepatocyte membranes.

2.)- Indirect pathway- transfer cholesterol to LDL & VLDL by cholesterol

transfer proteins.

*Hydrocholothiazide - I line T/t for HTN with osteoporosis (since it increases the
Serum calcium) and Isolated Systolic HTN.

*Epinephrine - Alpha1, Beta1 & Beta2 agonist.

*Nor-epinephrine - Alpha1, Beta1 Agonist.

*Niacin MOA - 1.) decreases the synthesis of hepatic triglycerides and VLDL ->
SUPPRESSED RELEASE of free fatty acids from peripheral tissues.

- 2.) decreases VLDL conversion TO LDL, thus decreasing LDL.

ADR - Flushing, Itching, increased Uric acid level, Hepatotoxicity, increased

insulin Resistance.

*Fibric acid derivative ADR- Gallstones, Myopathy.

*Fibrates and niacin - decrease hepatic VLDL production. Thus mainstay of T/t for
Primary hypertriglyceridemia (increased VLDL).

*EZETIMIBE - decrease absorption of dietary cholesterol-> decrease serum LDL.

*ApoB 100 - Apoprotein on VLDL &LDL. Decreased serum concentration of these will
cause decreased ApoB 100.

*Bile acid binding resins ADR- GI Upset, Hypertriglceridemia, Malabsorption.

*Isolated Systolic HTN T/t -

in Non-diabetics -Thiazide diuretics, Dihydropyridine CCBs

in Diabetics- ACE-I or ARBs

*Verapamil - diphenylalkylamine CCB.

- For rate control in AF with rapid ventricular response d/t ability to slow
conduction through the AV node.
ADR- Constipation and gingival hyperplasia.


MOA- 1. alpha-1 mediated Increased IP3 in visceral & cutaneous

vessels causes vasoconstriction, causing decreased blood flow to renal and hepatic
circulation n increased venous return.

2. beta-1 mediated cAMP increase in heart muscles through Gs

receptor mediated coupling. It increases cardiac muscle contractility, conduction
and heart rate.

*Terazosin, Doxazosin - Alpha-1blocker. Cause relaxation of smooth muscles in

arterial and venous walls-> decreases TPR.

ADR- first dose orthostatic hypotension & vertigo.

Hydrocholorthiazide - acts at DCt, prevents the reabsorption of sodium , chloride

and water by blocking Na/Cl cotransporter.

ADR- elevation of glucose, calcium and uric acid.

*Cardio selective beta blocker - pts. With coronary artery Ds. with CHF and HTN

*ACE-I - increase in Serum creatinine by 30% within 2-5 days is common, which
stabilizes in 2-3 weeks.

*Phentolamine - non-specific alpha-1 and alpha-2 blocker

*Atropin - competitive antagoinst at post junctional muscarinic receptors in the

heart. Atropin increases the heart rate by blocking vagal influences.

*Epinephrine - Increases Systolic BP- Alpha-1 & Beta-1

- decreases Heart rate - Beta-1

- decreases diastolic b.p. (low dose) - alpha-1<beta-2

- increases distolic b.p. (high dose) - alpha-1>beta-2

*Cilostazol & Dipyridamol- decreases the activity of platelet phosphodiesterase->

decreases the breakdown of cyclic AMP-> increased platelet cyclic AMP-> decrease
platelet aggregation by preventing platelet shape change and granule release.

- Cilostazol is also arterial vasodilator.

- cilostazol is approved for T/t of intermittent claudication.

*Ticlopidine & Clopidogrel - block platelet ADP receptor-> disllow GP IIb/IIIa receptor-
> inhibit platelet aggregation.
*Abciximab - monoclonal antibody that inhibits platelet aggregation by targeting the
platelet IIb/IIIa receptor.

- used prior to percutaneus coronary intervention.

*Bile acid binding resin (Cholestyramine) increases the bile acid production, thus
increasing hepatic triglyceride & VLDL production.

*Tachyphylaxis - rapidly declining effect of a drug after few days of use.

eg.- 1.) alpha adrenergic agents used as nasal decongestant. use >3 days
causes negative feedback, resulting in decreased norepinephrine synthesis and
release from nerve endings, resulting in relative vasodilation. It is rebound
rhinorrhoea/ rhinitis medicamentosa.

2.) Nitroglycerine- decrease in effect d/t diminished release of NO from target

cells. drug free intervals of 8-10 hours should be maintained during the use of
nitroglycerine to prevent tachyphylaxis.

*ACE-I - angioedema d/t Kinin accumulation is rare but serious ADr.

*Urticaria - IgE mediated mast cell degranulation.

*Regulation of RAAS involves 3 major pathways:- macula densa, intrarenal

baroreceptor and beta-adrenergic receptor pathway. in particular, the beta-
adrenergic pathway is mediated through sympathetic stimulation of beta-1
receptors located on Juxta glomerular cells. norepinephrine binds to beta-1
receptors and stimulates rennin release.

*Beta blocker- lowers b.p. by reducing cardiac output secondary to negative

chronotropic and inotropic activity.

*Loperamide- Opiate antimotillity drug, for travelers diarrhea, where there is no

fever or blood in stool.

*Erythromycin- for Campylobacter jejuni. in lieu of fluoroquinolones.

*Types of collagen - Strong, Slippery, Bloody and BM

1. Strong:- bone, Muscle, Fascia, cornea, Tendon, skin. Dentin.

2. Slippery:- Cartilage, Vitreous
3. Bloody:- Blood vessels, granulation tissue, Uterus, Fetal tissue
4. BM:- Basement Membrane/ Basal lamina.

*Glucocorticoids- High doses are used for ophthalmopathy A/w Graves Disease.
They are helpful in decreasing the severity of inflammation and decreasing
extraocular volume. Conventional antithyroid drugs do not improve
* SERMs- Tamoxifen, Raloxifen. Agonist in Uterus and antagonist in Breast.

- Antagonist in breast, thus, doesnt cause breast cancer.

-Agonist in Uterus thus can cause endometrial hyperplasia, endometrial

carcinoma and endometrial polyps. Thus the pt is advised to have annual
gynecological examination.

- Also improve the lipid levels and partial agonist to bone, thus increase BMD.

* Thiazolidinediones (TZD):- decreases insulin resistance by binding to peroxisome

proliferator activated receptor Gamma (PPAR-gamma), which is a transcriptional
regulator of genes involved in glucose and lipid metabolism.

- PPAR-Gamma belongs to nuclear receptor superfamily, which that includes

thyroid hormones also.

- TZDs take days to weeks to show significant effect.

TZD ADR- fluid retention causing CHF and weight gain.

Transactivation- when TZD binds to PPAR-gamma, a conformational change

ensues, which allows another co-activator to attach. This complex then binds to
transcriptional regulatory sequence of genes responsible for glucose and lipid
metabolism. This whole process is called Transactivation.

-Adiponectin (Adipocytokinin) levels are low in type 2 DM. T/t with TZDs
increases its levels.

*Important genes that are altered by PPAR-gamma :-

W Increases Adiponectin
W increases fatty acid transport protein
W increases insulin receptor substrate
W increases glucose transporter-4 (Glut-4)

*Desmopressin:- To treat Central DI and nocturnal enuresis.

- increases circulating levels of von Wille brand factor (factor VII:R) and
promote the coagulant activity of factor VII:C.

*Neutrophil count increases post corticosteroid administration, as a result of

demargination of leucocytes previously attached to the vessel wall.

*Glucocorticoids decrease eosinophil, basophil and lymphocyte count.

-T Lymphocytes are reduced more than B lymphocytes.

- reduction in lymphocytes occur by redistribution of lymphocytes from the
intravascular compartment to the spleen, lymph nodes and bone marrow. Also,
direct inhibition of immunoglobulin synthesis and stimulation of lymphocyte

* Premature Ovarian Failure- amenorrhoea, hypoestrogenism and elevated serum

gonadotropin levels in women age<40.

* Glucocorticoids increase liver protein synthesis, specifically the enzymes involved

in gluconeogenesis and glycogenesis.

* Glucosidase inhibitor decrease the activity of disaccharides on the intestinal

brush borders.

Eg.- Acarbose, Miglitol.

*Glucagon like polypeptide-1 (GLP-1) Incretin hormone secreted by intestinal L

cells in response to food intake. It decreases glucose by inducing satiety, decreasing
gastric emptying and increasing insulin resistance.

- acts through G-protein coupled cell surface receptor, which act by adenylate
cyclase activation.

* Biguanides eg. Metformin. Increases glycolysis and inhibits gluconeogenesis.

th* Amiodaron ADR:- Thyroid dysfunction, corneal micro-deposits, blue-grey skin

discoloration, drug related hepatitis and pulmonary fibrosis.

* Amiodaron induced HypOthyroidism- in iodine-sufficient regions.

T/t- levothyroxin and amiodaron continued as such.

*Amiodaron induced thyrotoxicosis- d/t excessive production of thyroid hormone.

- Primarily seen in iodine-deficient regions.

* NPH (neutral protamine Hagedorn) Insulin- intermediate acting insulin.

- crystalline suspension of insulin with protamine and Zinc, which prolongs

the duration of absorption of insulin. Thus increasing its duration of action.

- starts working in 2 hours, peaks in 4-12 hrs and lasts about 18 hours.

* Detemir- Long acting insulin analogue with a fatty acid bound to 1 of the lysine
amino acid on the insulin molecule. This fatty acid side chain allows the detemir to
bind to albumin and slowly dissociate afterwards, resulting in prolonged action.

- it usually starts working in with-in 2 Hours, peaks in 3-9 hours and lasts
about 24 hours.
*Beta-blocker- initially increases the PVR as it blocks beta2

*Metoprolol- Beta-1 blocker. inhibits renin release

*NO-> stimulates gunylate cyclase to convert GTP to cGMP-> decreased

intracellular Calcium concentration-> decreased activity of myosin light chain
kinase-> myosin light chain dephosphorylation-> smooth muscle relaxation.

*QRS complex corresponds to ventricular depolarization, in which rapid Na

movement in cardiac myocyte.

*ANti arrhythimic drugs do not affect phase 4 (the resting membrane potential) of
myocyte, but these do affect the phase 4 of pacemaker cell action potential, which
is mediated by Na influx.

*Digitalis ADR- fatigue, blurry vision, changes in color perception, nausea &
vomiting, diarrhoea, abdominal pain, headache, confusion, dizziness and delirium.

*Digoxin-> Stimulates Vagus-> increased parasympathetic tone-> decreased rate of

AV conduction-> AF controlled

*Methotrexate- ADR- Stomatitis( mouth ulcer), hepatotoxicity, myelosuppression,

increased risk of opertunistic infection, B-cell lymphoma and pulmonary fibrosis.

*Agents inhibiting purine and pyrimidine synthesis- MTX, leflunomide, azathioprine.

*After conversion to Dihydrotestosterone, androgens promote both follicular

epidermal hyperproliferation and excessive sebum production.

*Drugs causing acne - Androgens, epidermal growth factor receptor inhibitors and

*Estrogen is main hormone responsible for groethh and development of malignant

Breast Cancer

- aromatase inhibitors(Anastrozole, Letrozole, Exemestane) are superior than

Tamoxifen for it's T/t.

*lactic acidosis - Metformin ADR

*Agranulocytosis - Sulfonyl urea ADR

*postural/orthostatic hypotension- Insulin

*lung fibrosis- Amiodarone, bleomycin, Mitomycin C, busulphan and methysergide.

*Adrenal Crisis- hypotension, Tachycardia and hypoglycemia with a history

consistent with adrenal isufficiency (vomiting, abdominal pain, weight loss and
T/t- stress doses of corticosteroids.

*T/t of DKA- preffered insulin is I/V Regular insulin.

*Levothyroxin- synthetic form of T4.

*Hirsutism- terminal hair growth in male pattern in female.

Causes- PCOs, Cushing syndrome, ovarian and adrenal tumour and idiopathic.

T/t-Anti-androgens (spironolactone), Flutamide(testosterone receptor

antagonist) and finastride (5-alpha reductase)

*Virilization- Hirsutism, in association with clitoromegaly, increased acne, muscle

mass, increased libido and voice deepening.

*Mitotane- adrenolytic drug used primarily for treatment of adrenocortical


*Metformin- decreases blood glucose by increasing glycolysis, decreasing

gastrointestinal glucose absorption and decreasing blood sugar gluconeogenesis.

ADR- GI upset and lactic acidosis.

C/I- renal failure, hepatic insufficiecy and hypersensitivity to metformin.

-should be avoided in CHF and alcoholics, as because of increased risk of

development of lactic acidosis.

*Antithyroid drugs MOA- Oxidation of iodine in thyroid gland, iodination of tyrosine

residues and coupling of iodotyrosine molecules (i.e. iodine organification and
coupling). All done by thyroid peroxidase.

eg.-Propylthiouracil, Methimazol.

ADR- Agranulocytosis(usually within first few weeks of therapy)

Management- drug is immediately discontinued and a white cell count with

diffrential is drown.

*PTU- decreases peripheral conversion of T4->T3, has a shorter half-life and is the
drug of choice in pregnancy.

*Propranolol- Beta blocker with additional peripheral T4->T3 conversion blocking


*Flutamide- non-steroid antiandrogen that comppetes with testosterone and DHT for
testosterone receptors.

-used with GnRH agonists for Prostate cancer.

*GnRH Agonists(leuprolide, Goserelin, Nafarelin and histrelin)- Decrease synthesis of
LH and FSH-> decrease stimulation of Leydig cells.

*Ketoconazole- weak antiandrogenthat decrease the synthesis of steroid hormones

in gonads and adrenal.

*Anastrozole- non-steroidal aromatase inhibitor.

- decreases peripheral androgen aromatization

- for postmenopausal women with breast cancer in whom greater source of

estrogen is the conversion of androstenedione from adrenal to estrogen, in liver,
muscles and fat.

*Ocular manifestation of Grave's thyrotoxicosis sometimes respond to corticosteroid

therapy, but not to beta-blocker therapy.

*Clindamycin- Against Bacteroides and Gr. +Ve cocci

ADR- Pseudomembranous colitis

*Gentamicin ADR- Vestibular and cochlear toxicity, Nephrotoxicity and

neuromuscular paralysis( with large doses or intrapleural administration).

*MTZ ADR- GI ad neurological(paresthesia and dizziness).

*Chloramphenicol- can lead to dose related (reversible) or dose independent(often

irreversible) pancytopenia.

*Heparin- binds and activates antithrombin III

*Cryoprecipitate- contains FactorVIII,XIII,vonWillebrand's factor and fibrinogen.

*Protamine sulphate- Heparin overdose.

*Rat Poison- Brodifacoun ( 4-hydroxycoumarin derivative)

*Lepirudin and Argatroban- Direct thrombin inhibitor, used for Mx of heparin induced

*Ticlopidine ADR- neutropenia, fever and mouth ulcer.

-CBC is monitored biweekly for first 3 months

*Unfractionated heparin has pentasaccharide chain long enough (>18 saccharide

units) to bind to both antithrombin and thrombin.

*Gardos channel ( calcium dependent K ion channel) blockers hinder the efflux of
potasium and water from the cell, preventing dehydration of erythrocytes and
reducing the polymerization of HbS.
*Hyroxyurea icreases fetal hemoglobin (HbF) synthesis by an unknown mechanism.

- HYdroxyurea is reserved for Pts. with frequent pain crisis.

*Cimetidine, Metronidazole, cotrimoxazoland warfarin inhibit the metabolism of

warfarin, so dose need to be reduced.

*Rifampin, Phenytoin and phenobarbitol are enzyme enhancer.

*At low doses, aspirin inhibits COX1 alone, whereas at high doses, it inhibits both
isoenzymes irreversibly.

*NSAIDs produce REVERSIBLE COX inhibition.

*Abciximab, Eptifibatide and tirofiban- Inhibits binding of platelet GP II/IIIa surface

receptors with fibrinogen and fibronectin i.e. the final step in platelet aggregation.

*Ticlopidine and Clopitogrel - inhibit ADP mediated platelet aggregation.

Uses- Following PCI and T/t of unstable angina and non-Q wave myocardial

*Heparin Induced Thrombocytopenia (HIT) T/t- Direct thrombin Inhibitor eg.Hirudin,

Lepirudin and Argatroban. Inhibition of all Heparins.


Efavirenz and Delaverdine.

- Dont need phosphorylation intracellularly to get activated.

ADR- Hepatotoxicity with encephalitis(In first 6 weeks of initiating medication)

and life threatening SKin

reactions eg. Stevens -Johnson, Toxic Epidermal Necrolysis(in first 18 weeks).

*Protease Inhibitor- prevents assembly and maturation of the virus.

*Enfuvirtide- HIV Fusion Inhibitor. Binds to the envelope GP41 of HIV-1 and blocks
conformational changes necessary for the fusion of viral and cellular membrane.

*Heparin increases thromboxinIII activity-> Activated Antithrombin III binds to

thrombin(Factor II), Factor Xa etc.

*LMWH has more activity against Xa than Unfractionated Heparin.

*CLopidorel and Ticlopidin- Inhibit ADP mediated platelet aggregation.

*Age-related Macular degeneration- T/t- VEGF inhibitor [ eg.Ranibizumab(prefferred

Humanized recombinant antibody), Pegaptanib]; laser therapy and phototherapy.
*Epidermal Growth Factor receptor inhibitor (eg. erlotinib, Gefitinib) - for T/t of Non-
small-cell lung cancer.

*Rituximab- Monoclonal Antibody against Glycoprotein CD20.

Uses- B-cell Lymphoma, Rheumatoid Arthritis

*Infliximab- Chimeric IgG1 monoclonal antibody to TNF-alpha.

Uses-Rheumatoid arthritis, ANkylosing spondylitis and Fistulizing Crohn's


*Interlukin-2 - Cytokin that aids in maturation and diffrentiation of T-cells to aid in

tumor cell destruction.

Uses- RCC and Melanoma.

*CML - cells express BCR/ABL.

*Imatinib- inhibits BCR/ABL protein Tyrosin kinase. thus inhibits the cellular
proliferation of BCR/ABL cells without inducing apoptosis.

- ORAL medication.

*Naturally occuring negative coagulants- Protein C, Protein S, Antithrombin III and

Tissue Pathway Factor Inhibitor(TPFI).

*Protamine- binds and chemically inactivates heparin.

*G6PD Deficiency anemia Precipitating factors:-


2.Drugs- Dapsone,Antimalarials,Sulfonamides



*Raltegravir- Integrase inhibitor. Disrupts the ability of HIV to integrate it's genome
into the host cell's chromosomes, thus preventing host cellular machinery from
being used to synthesize HIv mRNA.

*Fusion inhibitor - Attaches to gp41 and ihibits virus entry into CD4+ cells.

eg.Enfuvirtide- binds to heptad repeat-1 (HR1) of gp41.

*HIV attachment to target cells is mediated by the binding of viral envelope protein
gp120 to the CD4 membrane protein of T-helper cells.
*RT inhibitor- HIV DNA Synthesis from RNA Template.

*Protease inhibitor- inhibits HIV polyprotein cleavage catalyzed by HIV VIral


*Integrase Inhibitor- inhibits HIV DNA integration into host genome.

*Aminocaroic acid and tranexamic acid- inhibit fibrinolysis. they inhibit plasminogen

*Ganciclovir - intgerfers to Human DNA, more tha acyclovir.

Use- CMV infection

ADR- Neutropenia, anemia, thrombocytopenia and renal dysfunction.

*AZT- can bind to and inhibit some mammalian cellularand mitochondrial DNA
polymerases, particularly beta and gamma polymerases.

ADR- Bone marrow suppression, causing anema, neutropenia.

*Samter's triad- asthma, aspirin hypersensitivity and nasal polyposis

- these symptoms occur due to the overproduction of leukotienes. As aspirin

blocks the Cyloxygenase pathway causing arachidonic acid metabolites to be
diverted into lipoxygenase pathway.

*Aspirin - at lowere doses increases uric acid levels.

- at high doses is uricosuric.

*Ascorbic acid - absorbed in distal small bowel by active transport

*pyridoxine (B6) - Jejunum, by passive diffusion

*Biotin (B7) & Pantothenic acid (B5) - via sodium dependent multivitamin

*Atrial Natriuretic Peptide & NO- act via cGMP.

*Penicillin - inhibits transpeptidase, the enzyme that catalyzes the final crosslinking
step in peptidoglycan cellwall formation.

*Penicillins - structural analogue to D-ala-D-ala

*Sulfonamides - compete with Para Aminobenzoic Acid (PABA) for incorporation into
folic acid.

*Cmompetitive antagoinist- Chnage ED50 to shift right, no change in Emax

*Non-Competitive antagonist- Change Emax to shift down, but no change in ED50

*Drugs with high intrinsic hepatic clearance tend to have high lipophilicity and a
high volume of distribution, with penetrance into the CNS and other tissues.

*NAPQI- N-acetyl-p-benzoquinoneimine, a Toxic and highly reactive metabolite of

Paracetamol by oxidation by Cyt P450. It is reduced by Glutathion.

N-acetyl cysteine(NAC)- Paracetamol poisoning Antidote. It acts as

glutathione substitute to bind to NAPQI.

- It also provides sulfhydryl groups to enhance the non-toxic sulfation

elimination of acetaminophen.

*MU Opiod Analgesic-> contraction of smooth muscle cells-> -> constriction and
spasm of of the Sphincter of Oddi-> Increased CBD pressure-> increased Gall
bladder pressure-> Billiary colic.

*Indinavir ADR- Lipodystrophy, Hyperglycemia and inhibition of CYP P450,

Nephrotoxicity and Nephrolithiasis.

*Foscarnet ADR-> Nephrotoxicity, Electrolyte imbalance(eg. Hypocalcemia,

hypomagnesemia and hypokalemia).

*Acyclovir ADR- Nephrotoxicity.

*TMP-SMX ADR- Megaloblastic Anemia, Stevens-Johnson Syndrome and TEN.

*the risk of CVA due to OCPs is very much increased in smokers and >35 Yrs.

*Absolute C/I for OCPs-

1. Prior H/o CVA or thromboembolic event

2. H/o estrogen dependent tumor

3. >35 Yrs. age

4. Hypertriglyceridemia

5. Pregnancy

6. DEcompensated or active liver diease(would impair steroid metabolism)

*Lead Poisoning-

1.Colicky abdominal Pain, constipation,headaches, impaired concentration

and deficits in short term memory.

2. Bluish pigmentation at the gum-tooth line.

3. Wrist drop d/t neuropathy

4. Microcytic hypochromic anemia and basophilic stippling on peripheral


Dx- blood lead level >10micro grams/ dL(0.48 micromol/L) on a venous


*Arsenic Poisoning- nausea, vomiting, abdominal pain, diarrhoea, decreased level of

consciuosness, hypotension, tachycardia and Garlic odor of breath.

T/t- Dimercaprol, which displaces arsenic ions from the sulfhydryl group of

*DImercaprol- narrow therapeutic range.

ADR- nephrotoxicity and Hypertension.

*CaNa2EDTA- Acute lead and mercury poisoning

*Methylene blue- Methemoglobinemia.

*OCPs- Primary mode of action is suppression of synthesis of the gonadotropins FSH

and LH, which there by leads to inhibition of ovulation.

- minorly, It also thickens the cervicle mucus making spermpenetration

difficult and progestrin prevents growth of the endometrium making it unsuitable for
implantation of embryo.

*Diphenoxylate- opiate anti-diarrhoeal. binds to GI Mu receptors and lowers motility.

ADR- Bloating and mild sedation.

*Octreotide- Helpful in secretory diarrhoea.

*Amantadine- impairs uncoating of Influenza-A virion after host cell endocytosis.

Ribivirin MOA- Lethal Hypermutation, inhibiting RNA polymerase and IMP (depleting
GTP), causing defective 5'-cap formation on viral mRNA transcript and modulating a
more effective immune response.

*Bioavailability = Area under the oral curve* IV dose/ area under the IV curve*oral

*Lyme disease vaccine- contains aa recombinant outer surface protein from Borrelia
burgdorferi bacteria

*Gout and pseudogout- WBC count <20,000

*Septic/Gonococcal arthritis- acute monoarticular arthrtis, with WBC count >50,000.

*Rheumatoid Arthritis- swelling, pain and morning stiffness in multiple joints for >6

T/t- Acute- Corticosteroids and NSAIDs.

Chronic- Methotrexate. It takes weeks to show effect.

*Hydrochlrothiazide- it increases the absorption of calcium from DCT within

nephrones. Thus causing Hypercalcemia and hypoclciuria.

*Etambutol ADR- optic neuritis causing visual acuity, central scotoma or color

*Aminoglycosides & Vancomycin ADR- direct damage to the 8th cranial nerve.
Therefore can cause deafness, vertigo and tinnitus.

*Aminoglycosides ADR- ototoxicity,Renal toxicity(Acute Tubular necrosis) and flaccid

paralysis due to neuromuscular blockade.

*CBC to be monitored in- Chloramphenicol(aplastic anemia),

Dapsone(agranulocytosis) and TMP-SMX(Megaloblastic Anemia)

*Bosentan- competitive antagonist of endothelin receptors.

- used for Primary Pulmonary HTN

*Etanercept- humanized monoclonal antibody against TNF-alpha

-anti-inflammatory agent indicated for treatment of Rheumatoid arthritis,

Psoriasis and Psoriatic Arthritis.

*N-acetylcysteine- a mucolytic agent that loosens the thick sputum by cleaving

disulfide bonds within mucus glycoproteins.

*Antimuscarinic agents (ipratropium,tiotropium) only reverse Vagally-mediated


*Methylxanthines(theophylline,aminophylline) cause bronchodilation by decreasing

phosphodiesterase enzyme activity, thereby increasing intracellular cAMP.

*Mycobacterium Avium Complex (MAC) T/t- Rifampin, Ethambutol and a

macrolide(azi or clarithromycin).

*Staphylococcal endocarditis- Penicillin and aminoglycoside

MRSA- Vancomycin, Rifampicin/aminoglycoside.

*Rifampin Monotherapy in exposure/carrier state of N. Meningitis.

*for Rifampin monotherapy bacteria rapidly acquire resistance through spontaneous
genetic mutations of the bacterial DNA-dependent RNA polymerase.

*aerosolised Ribavirin- for RSV infection, espacially in infants and children who are
at risk for disease progression.

*Oseltamivir- SIalic acid analogue inhibitor of Influenza A and B viral


*Ganciclovir- Anti-CMV guanine nucleoside analogue.

*Isoniazid MOA- inhibition of mycolic acid synthesis after activation by bacterial


Resistance- through non-expression of the catalase-peroxidase enzzyme or

through genetic modification of it's binding site on mycolic acid synthesizing

*Ethambutol- MOA-> inhibits with bacterial cellwall.

Resistance- Mycobacteria increase production of arabinosyl transferase (an

enzyme that polymerizes arabinose-> arabinan-> arabinogalactan)

*Pyrazinamide- converted to pyrazinamic acid, causing acterial environment to

become acidic.

Resistance- decreased activity of mycobacterial enzyme pyrazinamidase.

*Amphotericin B- MOA- binds to ergosterol with higher affinity than with cholesterol.

Toxicity- 1. Acute infusion related reactions. these decrease with subsequent


2. dose dependent nephrotoxicity- coz it decreases the glomerular filtration

rate. KFT should be closely monitored.

3. HYpomagnesemia and hypokalemia. within first week of infection.

4. Anemia- d/t decreased renal erythropoietin synthesis. severe with AZT.

5. Thrombophlebitis.

*C. dephtheriae- causes bacterial toxin mediated axonal damage.

*Isoniazide is structurally similar to pyridoxin (B6). as a result it increases the

urinary excretion of B6. also, it competes with B6 binding sites, leading to the
defective synthesis of neurotransmitters like GABA.
*Antibiotics that act on 50S ribosomal subunit- chloramphenicol, clindamycin,
linezolid and macrolides.

*Antibiotics that act upon 30S subunit- Tetracyclins, doxyxycline and


*Varenicline- Partial agonist of alpha4 beta2- nicotinic acetylcholine receptor.

- reduces withdrawal cravings and attenuating the rewarding effects of


*MAc infection- <50 CD4 cells.

-more involvement of RES causing Fever, weight loss diarrhoea, anemia,

hepatosplenomegaly, and elevated LDH and ALP levels.

- MAC grows well at higher temperature(unlike TB)

T/t- Azithro/clarithro with rifabutin/ethambutol.

Prophylaxis- weekly Azithro and pharamcological HIV T/t to bring CD4 cells

*Cromolyn and nidocromil- for prophylaxis in seasonal asthma, exercise induced

asthma and aspirin hypersensitivity.

*Lukasts- chronic asthma prophylaxis.

*Mycolic acid- long branched chain saturated fatty acid that contain aproximately
ninety carbon molecules.

*Polyenes(Amphotericin B and Nystatin):- bind ergosterol molecules in fungal cell

membrane, forming pores and causing cell lysis.

*Triazoles(keto,itra,flu and voriconazole):- inhibit ergosterol synthesis.

*Echinocandins(Caspofungin and micafungin):- inhibit 1,3-beta-d-glucan synthesis, a

component of fungal cellwall.

- Maximum activity against Candida and aspergillus, limited activity against

mucor and rhizopus and no activity against Cryptococcous neoformans.

*pyrimidines (Flucytosine):- convorted to 5FU and interferes with fungal RNA and
protein synthesis.

*Griseofulvin- enters fungal cells, binds microtubules and inhibits mitosis.

-effective only against dermatophytes, as it gets accumulated in keratin

containing tissues.
*Terbinafin- inhibits squalene-2,3-epoxidase, which ultimately results in in decreased
synthesis of ergosterol.

*Pyrazinamide- Acts in acidic media, so works better on intracellular organism

engulfed by macrophages.

*Isoniazid, ethambutol and rifampin - activity against extracellular organisms.

*Theophyllin Toxicity- abdominal pain, vomiting,, diarrhoea, cardiac

arrhythmias(tachyarrhythmias) and seizures(major cause of morbidity and

T/t- beta-blockers for tachyarrhythmias.

- theophyllin induced seizures are very difficult to treat. BZD and

Barbiturates are used.

*Stretomycn- Uses-> Plague, Tularemia and TB.

*Medications causing Seizures- Bupropion( with H/o seizures and bulimea/anorexia

Nervosa), Ciproflox, Clozapine(antipsychotic, at high doses), Isoniazid( anti-
ttubercular, if given without pyridoxin) and imipenem.

* Clozapine ADR- Agranulocytosis

*Bone Marrow suppression - by Carbamazepine and Valproate.

*Lamotrigine- Rash, may even cause Stevens-Johnson.

*Olanzapine- Wt. gain.

*Sexual dysfunction - SSRI.

*Malignant hyperthermia- AD trait. Abnirmal ryanodine receptor, which are Ca

channels. these kept open in influence of some agents-> high influx of Calcium ion-
> excessive consumption of ATP-> excessive generation of heat-> both these slong
with ATP depletion cause muscle damage(rhabdomyolysis)-> releases potassium,
myoglobin and creatin kinase in the circulation.

Causative agents- Inhalation Anaesthetic(esp. Halothane) and muscle

relaxant Succinylcholine.

T/t- Dantrolin.

*Myasthenia Gravis- Dx- edrophonium

T/t- Neostigmine, pyridostigmine

*ADPKD- may have Berry aneurysm.

*No earlier than 3 days post SAH (usually 7-8days), pt may show signs and
symptoms of cerebral vasospams i.e. altered mental status and focal neuronal

T/t- Nimodipine as preventive medicine.

*Physostigmine- Tertiary amine, which can cross BBB and reverse the anti-
muscarinic effect of Atropin.

*Neostigmine and edrophonium- quarternary amines, so can not cross BBB.

*Diazepam- Used as muscle relaxant to to stop spasticity caused by UMN disorders

(eg. MS, Strokes, Spinal cord trauma) and tetanus.

*BZDs- should not be co-administered with alcohol, barbiturates, neuroleptics and

Igeneration antihistamines.

*Penicillines irreversibly bind to PBPs eg. transpeptidases.

*Opiods- No tolerance to Mitosis and Constipation.

*Phenytoin -> MOA- inhibits neuronal high frequency firing by reducing the ability if
sodium channels to recover from inactivation, increasing the refractory period.

uses- tonic-clonic and psychomotor seizures. seizure Prophylaxis after head

trauma and before neurosurgery.

ADR- Generalized Lymphadenopathy(Pseudolymphoma), cosmetic

effects( Hirsutism, coarsening of facial features, acneiform skin rash and GINGIVAL

*Carbamazepine- Uses- GTCS, Partial Seizures, pain relief in trigeminal and diabetic
neuropathy and bipolar disorder.

ADR- Agranulocytosis.

*Valproate- ADR-> Hepatotoxicity.

*Phenobarbitol ADR- Acute Intermitent Porphyria.

in toxic doses- sedation or cardiovascular and respiratory depression.

*Vitamin B6 increases the peripheral metabolism of Levodopa decreasing its


*Serotonin Syndrome- COnfusion, agitation, Tremor, Tachycardia, Hypertension,

Clonus, Hyperreflexia, Hyperthermia and Diaphoresis.

Causes- COmbination of SSRIs and MAO-Inhibitors, High doses of SSRI.

T/t-Supportive Care, Cyprohepatidine, a first generation histamine antagonist
with non-specifi 5HT1 and 5HT2 receptor antagonist properties.

-Short acting antihypertensives acn be used to treat hypertension a/w

serotonin syndrome. HYpertensive agents with longer half lives, should be avoided
d/t risk of developing hypotension and shock.

Haloperidol- antipsychotic. it's adverse reaction is similar to Serotonin


BZD- used to releive agitation, mildly reduce HR and b.p.

*Aged Pt.s with H/o falls etc., should not be given first generation antihistamines.

*Alzheimer's Disease- CNS NMDA receptor overstimulstion by glutsmate may

contribute to AD.

T/t- Cholinesterase Inhibitor(Donepezil), Antioxidents( Vit. E) and NMDA

receptor Antagonist( Mementine).

*GABA- BZDs bind to allosterically to gaba chloride ion channel and increase the
frequency of Cl ion channel opening. Thus facilitates GABA actions.

-Barbiturates- prolong the duration of ion gate opening in response to GABA.

AT higher concentration, they open the ion gates without need of GABA.

*Bupropion- ANtidepressant that doesn't cause sexual dysfunction.

ADR- agitation,insomnia and seizures.

-doen't significantly influence serotonin, Ach or histamine.

Uses- depression with accociated psychomotor retardatio or hypersomnia.

-Also effective in treatment of nicotine dependence.

*Ethosuximide - Absence Seizures.

- blocks T-type calcium ion channels that trigger and sustain rhythmic pulsed
discharges in thalamic neurons.

*Phenytoin - GTCS, STatus epilepticus.

- inhibits neuronal firing of action potentials by blocking Sodium ion channels

*Carbamazepine- COmplex Partial seizures and GTCS.

ADR- Apllastic Anemia and Agranulocytosis.

*Entacapon- Peripheral Catechol-o-methyl-Transferase (COMT) inhibitor.

*Talcapon- Peripheral and central COMT inhibitor.

- Hepatotoxic.

*Selegiline- inhibitor of brain's MAO-B, decreases central dopamine degeneration.

*Anti-cholinergics, like Trihexyphenidyl and Benztropine, inhibit central muscarinic


-Mainly used for Parkinson's Disease.

*TCAs ADR- Urinary Retention (competitively block Ach on muscarinic receptors of

bladder),Cardiac arrhythmia(quinidine like effect, QRS and QT prolongation),
Seizures (in CLomipramine), Orthostatic Hypotension (through alpha-adrenergic
blockade) & sedation (d/t bloackade of Histamine receptors)

* Seizures - ADR of CLomipramine and Bupropione( DOpamine-Norepinephrine

reuptake inhibitor)

- D/t antihistaminic, antimuscarinicand anaesthetic properties.

*MAO Inhibitors- Tranylcypromine, phenelzine, Selegiline.

*Drug Induced parkinsonism- By Dopamine(D2) Receptor blockade in the

nigrostriatal pathway. Usually occur with first generation anti-psychotics.

T/t- Anticholinergics (like Benztropine, Trihexyphenidyl).

- Levodopa and dopamine agonist can exacerbate Psychosis, so C/I in drug

induced parkinsonism

*Buspiron- Selective agonist of the 5HT1a receptor.

-Anxiolytic with Minimal to no Hypnotic, sedative or euphoric effects.

- Dependence doesn't occur, even with chronic use.thus can be used in Pts.
with h/o of abuse of anti-anxiety drugs.

- Clinic response strats in 2 weeks.

*Negative symptoms of Schizophrenia respond poorly to the antipsychotic

medication. Psychosocial treatments, such as congnitive behavior therapy are
effective in treating these.

*TCAs- Used for Diabetic Neuropathy

*Bupropion- Uses- Major depression, tobacco dependence and hypoactive sexual

-Structurally related to amphetamine and inhibit presynaptic reuptake of
Dopamine and NE, with greater effect on Dopamine.

ADR- Seizures, pts with H/o seizures, bulimia/anorexia.

* Cisplatin- MOA- forms a reactive oxygen species that can form Crosslinks.

ADR- Acute Tubular Injury.

Amifostine - a thiol based cytoprotective free radical scavenging agent

used to decrease the cumulative nephrotoicity associated with platinum containing