Drugs Pharmacology

Anti Hypertensive Drugs

Name MOA Pharmacology Toxicities/SDFX Reflex Contraindications Administration Misc

Brain

DM, Hypokalemia

Loop (Furosemide/Lasix) DM, Hypokalemia

RAAS Ihibiting Drugs


w NSAIDS = HTN

Diuretics - DOC x HTN monotherapy

↓ plasma volume ECFV → ↓ VR → ↓ CO → ↓ MAP/BP → ↑ TPR (Reflex) → ↑ PRA → ↑ CO → a maintained lowered TPR; 1) ↓ intravascular volume and 2) ↓ vascula responsiveness by ↓ Na and ↓ Ca++

Drug Drug Interactions

Thiazides (Hydrochlorothiazide/HydroDiuril/H2TZ)

Work on Distal convoluted Tubule (descending loop of Henle?)

Sexual Dysfunction, hypovolemia, Hypokalemia/alkalosis, Hypomanesemia, Hypercalcemia, Hyperuricemia, Hyperlipidemia, Hyperglycemia

w Quinidine=Torsade de Pointes; w Digoxin= Dig Toxicity; w Cotricosteroids=↑ Na Retention; w Li=↑ Plasma [Li]; w Warfarin=↓ effectiveness; w NSAIDS=HTN

Elderly or dehydrated or other RxRx interactions; DM, Hypokakemia

may need K supplements; ↓ in K → ↓ BP and ↑ arrythmias

Along w tx HTN Diuretics (in general) are good for Edema, Dyspnea; Thiazides are good x Severe Renal Impairment w HTN

Thiazide-like (Chlorthalidone/Hygroton)

blocks Na/2Cl-/K on Ascending Loop of Henle so they stay in lumen

Hearing Loss (just like aminoglycosides), Hypocalcemia

good x tx of HTN w Renal Impairment even morese than Thiazides

K-Sparring (Spironolactone, Eplerenone/inspra)

Aldosterone receptor antagonist; Reduce aldosterone levels?

Estrogenid SDFX/Gynecomastia b/c of steroid like sx of drug;

NSAIDS, β blockers and ACE inhibitors ↑ Hyperkalemia; may lead to cardiac arrest

good x tx of HTN w Hypkalemia


ACE Inibitors (end in -pril eg Captopril)

Block A I: A II conversion in lung endothelial cells; ↑ Bradykinin

↓ A-II prodx → ↓ TPR and ↓ aldosterone and ↑ Na excretion; ACE breaks down bradykinin, so if it's blocked the bradykinin can stick around longer

Captorpril causes rash; hpotension, Na depletion; Dry cough → ↓ compliance, Hyperkalemia bc K not excreted bc aldosterone is inhibited; Angioedema (esp if black); Renal Failure due to ↑ GFR, Proteinuria, rashes (captopril) fever, pancytopenia, BM depression

Great Results If Used w Thiazides

Little sex dysfx SDFX; help manage DM; ↓ mortality if prior MI; only antihypertensive mx w/o sexual dysfx

Angiotensin II Receptor Blockers/ARB's (end in "-sartan"; Losartan, Valsartan, Irbersartan, Candesartan, Telmisartan, Eprosartan)

Block AII type I receptors → ↓ aldosterone relaease and vaeesel relaxation

↑ bradykinin → angioedema

Aldosterone Receptor Blocker (Spironolactone, Eplerenone)

Sympathoplegic AgentsCNS α2 Agonists; Ganglionic Blockers; Neurotransmitter Depletors; α, β, Blockers


↓ HR, VR, TPR, CF none :)

↓ HR, VR, TPR, CF

β blocker-Labetolol β1, β2, α1 blocker no reflex tachycardia DM, Asthma, CHF

Angina

Ca++ Channel Blockers


α2 Agonists (Clonidine, Guanabenz)

some orthostatic hypotension; Dry Mouth, Drowsiness, Depression; Sexual Dysfx; Withdrawl Supersensitivity; Pseudotolerance

Ganglionic Blockers (Trimthapham Camsylate)

Orthostatic Hypotension; Sexual Dysfx; Paralytic Ileus, Urinary Retention (esp old men)

Vasodilation w/o reflexes (cool)

Sympatholytic Agents (Reserpine, Guanethidine, Guanadrel)

Deplete adrenergic neurotransmitters

Reserpine: Suicide, depression, ↓ sypmathetic action. Guanethidine: Retrograde Ejaculation. Orthostatic Hypotension, Fluid Retention, Sexual Dysx; Parasympathetic Predominace (Nasal Stuffiness, GI acid secretion, Diarrhea, Bradycardia); Supersensitivity

OTC decongestants; pts w hypokalemia (b/c diarrhea causes K loss); Reserpine depression

Reserpine is cheap and effective but as HORRIBBLE SDFX

α blockers (Doxazosin, end in "-sin")

pts using Doxazosin were 25% more likely to have hrt falu

β Blockers (end in "-ol", Nadolol, Propranolol, Timolol, Atenolol, Bisoprolol, Metoprolol, Labetalol)

↓ CO via ↓ HR and CF; ↓ CNS; ↓ RAAS (no compensatory volume expansion

Bronchospasm (esp nonselective), Hrt Failr; Bradycardia; AV block; Peripheral Vascular Diss esp in Raynauds: Depression (not as bad as Reserpine); Vivd Dreams; Sex Dysfx

α response → ↑ TPR and VR; Atenolol ↑ TPR (reflex)

NonSelective β blockers - Asthma, Vascular Disease

Esp good in white ppl w hyperkinetic hearts; Esp good for Ventricular Ectopies, Angina, Sinus Tachycardia and Dissecting Aneurysm

↓ TPR, HR, CO, VR (basically ↓ sympathetics)

Orthostatic Hypotension, Bradycardia, Heart block, ↓ CF

Vasodilators (Hydralazine, Minoxidil, Diazoxide; Nirtoprusside))

↓ TPR Hydralazine Minoxidil Diazoxide: ↓ TPR and VR Nitroprusside

Hydralazine SLE esp in slow acetylators ≤ 200mg/day, Rapid Drop in TPR → angina; Minoxidil Hair growth

↑ K channel efflux → ↓ excitability → ↓ arterial reactivity/constriction; ↑ blood volume, ↓ in venous capcitance; ↑ TPR, ↑ HR, ↑ contractility

Nitroprusside (IV only); Others oral

SDFX = ↓ TPR (all), ↓ HR (V,D>>N), ↓ CF (V>>D,N)


OK to use w β blockers

Tachycardia β blockers

All antihypertensive mx cause ↑ in RAAS (via: ↓ BP and CO → ↓ blood flow to kidney → ↑ RAAS), ↑ chance of Orthostatic Hypotension (via ↓ contractilty, volume or CF).

Dyslipidemia Drug Therapy


Nicotinic Acid/Niacin Inhibits adipose Lipase

Type I hyperlipidemia


Phenylalkylamine (Verapamil)

constipation, Hypotension, some HA, Peripheral Edema (no RE to diuretics), AV block, some CHF

β blockers; Cardiac Failure

Benzothiazipine (Diltiazem)

a little hypotension, peripheral edema, AV block (nyeh)

considered the safest Ca channel blocker

Dihydropyridines (Nefedipine et al)

Hypotension, HA, Peripheral Edema (does not RE to diuretics)

w β blockers → ↓ HR THIS IS BAD!

sublingual, short duration

highest affintiy x heart of other Ca chnl blkrs; good in ER situation


Reduces esterificationof TG in liver, May reduce hepatic cholesterol formation, Reduces VLDL, TH and LDL, ↑ HDL, Effective vs Hyperlipidemia Types II-V, Cho-ol levels reduced ≈ 25% @ 3gm/day. ↓ clotting via ↑ tissue plasminogen factor and ↓ plasma fibrinogen

Flushing, Pruitis (itching), Abdominal pains, Dyspepsia Peptic ulcers (at first), Hepatic dysfx (jaundice, ↑ transaminase levels)

Give w Aspirin; Use in pts w ↑ ↑ TGs

Poor pt compliance; Use in pt w ↑ ↑ TGs

Fibrates (Gemfibrozil)

↓ serum TG, ↑ extrahepatic LPL, ↓ aplipoprotein synths, ↑ HDL?

↑ extrahepatic lipoptotein lipase (LPL), ↓ aplopotrotin syths, ↓ serumTG, ↓ VLDL, kinda ↑ HDL; ↓ plasma fibrinogen levels :: Gallstones, ↑ chance of arrythmias, Nausea, Cramps, Bleeding due to ↓ platelet adhesiveness → bleeding

w Statins = ↑ chance of Rhabdomyolysis

Use x pts w TH >750mg/dL, esp good if pt is Type III (elevated IDL) phtyp

Indicated x pts w TG>750 mg/dL; esp good x Type III hyperlipidemia; Not good x pts w Type I; Ppl use x ↑ in surviival w/o evidence.

ANTICOAGULANTS

Antithrombotics


Aspirin

GP Iib/IIIa Inhibitors IV ONLY

ABCIXIMAB GP Iib/IIIa Inhibitors IV ONLY

EPTIFIBATIDE GP Iib/IIIa Inhibitors IV ONLY

Tirofiban GP Iib/IIIa Inhibitors IV ONLY

Anticoagulants (prevent fibrin scaffold formation after platelet aggregation)


Bile Acid Sequestrants (Cholestyramine, Colestipol, Colesevelan)

Binds bile acid which are precursors to cholesterol which shifts bile acid prodx instead of cholesterol

↓ LDL, Not absorbed in GI tract,

Major Constipation, impaction, abd cramps, Hemrrhoid aggrevation

Absorbs other drugs as well as bile acids so Cholestyramine will also bind vitamins, digoxin etc

Stagger administration of other drugs

Chlestipol & Colesevelan are newer and more potent w less SDFX and help ↓ CHD mortality and ↓ major coronary events

Cholesterol Absorption Inhibitor (Ezetimibe)

↓ cholesterol absorption from guy → ↓ cholesterol, ↓ TG

Diarrhea, Hepatic insuffx; These SDFX are mild/more tolerable vs BASeqeuestrants

HMG CoA Reductase Inhibitors ("Statins")

inhibit HMG CoA Reductase → ↓ cholesterol synths

Works in liver, ↓ cholesterol, ↓ LDL, ↑ HDL

Myalgias, rhabdomyolysis (rare)

NEVER USE IN PREGNANT WOMEN

Good Compliance but Expensive; Must Perform LFT bf and after tx


Stroke, Hemorrhage, Bleeding, GI Distress, ulcers

Aspirin is used to help prevent thrombus formation; used to help prevent 2nd stroke. NOT useful to prevent 1st seizure

ADP Inhibitors (Clopidogril)

irreversibly inhibits ADP prehibiting platelet aggregation

DOC x preventing 2ndary stroke or MI

Bleeding of hemorrhage, easy burising, GI, Intracranial

Used during invasive cardiac procedures CABG, PTA

Inhibit fibrinopen receptor on platelets to inhibit fibrin binding and scaffold forming

Bleeding, immune reaction

Inhibit fibrinogen receptor on platelets to inhibit fibrin binding and scaffold forming

Bleeding immune reaction

Inhibit fibrinogen receptor on platelets to inhibit fibrin binding and scaffold forming

Bleeding,


Heparin

Enoxaparin

Warfarin/Coumadin

Thrombolytic AgentsDissolve clots by activating the conversion of plasminogen to plasmin that hydrolyzes fibrin. Therapeutic window 2-6 hrs after ssx usu IV


Streptokinase Activates Plasminogen Thrombo-Embolic Stroke IV ONLY

Binds to Antithrombin III thus preventing inactivation of thrombin.

HMW Heparin binds to AT III bound to factor Iia or Xa. LMW heparin binds to ATIII bound to XA only

Spontaneous hemorrhage, alopecia, HSS, fever, skin ncrosis osteoporosis/sponatneous bone brkg @ chronic doses, dangerous ↓ lvls of AT III, thrombocytopenia, antiplatelet AB's

pts w religious wishes against pork (it comes from pig glycosaminoglycans)

Do NOT Give Orally. Do NOT Give IM.

Does not cross BBB or placenta. Treat spontaneous hemorrhage w protamine sulfate

Direct Thrombin Inhibitors (Hirudin Argatroban)

Inhibit Thrombin (Factor Iia)

by inhibiting Factor Iia it stops fibrin from being made, and prevents scaffold formation; Lepirudin/Hirudin is used to replace Heparin in Heparin-Induced Thrombocytopenia; Argatroban is used to tx Heparin induced Throbocytopenia

prolongs PTT (so does Heparin)

Lepirudin is derived from leech saliva

DOC x DVT prevention after hip surgery

Stops the reduction of vit K.

Reduced vit K is crucial x turning Preprothrombin into Prothrombin thus the Ca++ on gamma Carboxyglutamic acid can't bind FIIa or FIXa to the platelets. -wiki; Warfarin is used to tx A fib, Prevent Thromboemboli stroke, acute MI, Venous Thromnosis and Pulmonary embolism.

↑ Warfarin activity if in conjunction w Cimetidine (OTC H2 blocker) via ↓ warfarin metabolism, w Phenylbutazone via ↓ binding to prots, w Aspirin = ↓ Platelet fx:: ↓ Warfarin activity if in conjunction w Cholestyramine due to ↓ absorption, Phenobarbital by inducing cyt450, w Phenytoin by inducing cyt450

pregnant women (crosses BBB and causes fetal death birth defects)

Oral (good good thing) w 100% bioavailability. Dose is calculated by finding INR PT so that PT ≈ 2.

cyto 450 metabolization; binds to prots.

How to treat SDFX: Mild bleeding w dose Reduction; Severe Bleeding w stopping regimen and give Vit k; BAD bleeding via all of the above w concentration or plasma


Thereapeutic window 2-6hrs after ssx. Used x DVT, Acute MI

Bleeding (antidote=AminoCaproic Acid), Immune Rxn, Fever, Anaphylaxis

t1/2=23 mins; NOT an enzx

IV

Desmoteplase IV

Aminocaproic Acid Used to tx bleeding

Protamine Sulfate antagonizes heparin Used to tx bleeding

Vitamin K Used to tx bleeding

Antianginal Drugs


AspirinThromblytics

Ranolazine

Effort angina + HTN? Treat w Ca Channel Blockers or β blockers. Effort Angina + Asthma/COPD? Treat w Ca Channel Blocker. Variant angina + HTN + Sinus Bradycardia? Treat w Nifedipine

Tissue Plasminogen Activator (Alteplase, Reteplase, Tenecteplase)

Alteplase repidly activates plasminogen bound to fibrin inthrombus (low affinity for free plasminogen); Urokinase

Thereapeutic window 2-6hrs after ssx. Used to tx MI (not better vs streptokinase), Thromboembolic Strokes(not that great); Alteplase is good @ treating MI (90 min window), Massive pulmonary embolism, Ischemic stroke (3 hr window)

GI and intracranial bleeding

Thereapeutic window 2-6hrs after ssx.

inhibits plasminogen activation

maybe intravascular thrombus

HSS, Dyspnea, Flushing, Bradycardia


Nitrates (Nitroglycerin, ISDN, ISMN)

Mimics endogenous NO ↑ the cGMP pathway which relaxes myosin. Effort angina - ↓ preload, SV MVO2; Variant angina- ↑ coronary flow by relieving coronary spasm; Mixed angina - ↑ coronary blood flow ↓MVO2

Dilates the viens>>coronary aa>>peripheral aa. Used to tx Effort Angina. ↓ Venous Flow → ↓ Preload → ↓ LVEDV/P → ↓ Ventricular stretch → ↓ Systole time → ↓ Stroke Volume → ↓ MVO2/Cardiac work → ↓ Venous Return…

Flushing of face neck, Pulsating HA due dilation of meninges (esp if topical) , Postural Hypotension due to antagonism of SAS, Halitosis, Methemoglobinemia

Sublingual to bypass liver, Oral, Topical (ointment ?looks like toothpaste?) Dispensed in Lactose to prevent combustion. Should have burning sensation when placed in tongue

Keep away from air, light. Tolerance develops to low doses @ ≈ 4 wks. Stagger w drug free periods to avoid tolerance

β Blockers (Nadolol, Propranolol, Timolol, Atenolol, Bisoprolol, Metoprolol)

↓ HR & CF → ↓ CO & MVO2

Use to tx Effort angina and Acute MI. Not that great x Variant angina

Bronchospasm (esp nonselectives), Heat failure, Bradycardia, AV Block, Peripheral Vascular Disese, Raynaud's, Depression, "Vivid" dreams, Sexual Dysfx.

maybe: ↑ LVEDV → ↑ Heart size → ↑ duration of systole → ↓ coronary perfusion → ↓ O2 delivery → ↑ O2 demand → reflex ↑ CF or HR. damn…

Calcium Channel Blockers (Verapamil, Ditiazem, Nifedpiine)

block voltage gated Ca channels esp in aa>>vv; Verapamil - ↓ HR, CF TPR and ↑ coronary flow; Ditiazem - ↓ HR TPR & coronary flow; Nifedipine - ↓ TPR & ↑ coronary flow

Used to tx Prinzmetal angina; Effort angina refractory to NO's/ β blockers, or pts w bad SDFX to β blokrs and NO's. Only Verapamil and Ditiazem are indicated x pure effort angina.

Ditiazem - AV block, Hypotension; Verapamil - Hypotension, HA, Periph Edema, Constipation, AV block, CHF; Nifedipine - Hypotension, HA, Perip Edema

Nifedipine has ↑ contractility and ↑ HR as reflexes

only Ditiazem is safe to use w β blockers

Oral, prot bound, No Orthostatic Hypotension

Coronary Vasodialtion - D, V, N); Peripheral Vasodilation - N, V; Contractility - N ↑ (reflex), V ↓; HR - D ↓, N ↑ (reflex) , V ↓

Fatty Acid Oxidation Inhibitor (pFOXI)

Antiarrhythmic AgentsClass I Na Channel Blockers (Impede Diastolic Depolarization at some point?)


Ia Procainamide IV

Ia Disopyramide

Ib Lidocaine IV Not as deadly as Ia

Ib Tocainide oral Not as deadly as Ia

Ib Mexiletine oral Not as deadly as Ia

Ib Phenytoin oral Not as deadly as Ia

Ic Flecanide Just as deadly as Ia

Ic Moricizine Just as deadly as Ia

Ic Propafenone Just as deadly as Ia

Class II - β Blockers



bind to open/active Na channel

↑ upstroke of AP duration (APD); ↓ K flow; ↑ phase 2, and AP depolarization

Fever, Rash, AntiNuclrAntibodies, K channel blocking, widen QRS cmplx, widen QT intervals; ≈ 20% converted to NAPA in liver so watch x NAPA toxicity, Lupus in slow acetylaters

↑ toxicity w Amiodarone Cimetidine Ranitidine Procaine

No evidence shows it works. Ia and Ic kill ppl.

bind to open/active Na channel

↑ upstroke of AP; ↓ K flow; ↑ phase 2, and AP depolarization

No evidence shows it works. Ia and Ic kill ppl.

bind to inactive/closed Na channel

↑ K flow, ↓ APDl and phase 2

Mouth numbness, Tinnitus, slurred speech, confusion, somnolescence, sxrs, CNS depression; activates K channels → ↓ AP duration from hyperpolarization

↑ toxicity w Propranolol, Verapamil Cimetidine


↑ K flow, ↓ APD and phase 2

activates K channels → ↓ AP duration from hyperpolarization


↑ K flow, ↓ APD and phase 2

activates K channels → ↓ AP duration from hyperpolarization


↑ K flow, ↓ APD and phase 2;

Death via Hypotension, Cardiac Failure, Asystole esp in old ppl, Teratogenesis, Gingival Hyperplasia, Hirsutism; activates K channels → ↓ AP duration from hyperpolarization

↓ upstroke of AP BIG TIME

All Class I antiaryhthmics ↓ Excitability, Responsiveness, and ischemia; also, by ↑ phase 2 they stop the cells from becoming prematurely "ready"/primed? for another contration. (except for lidocaine). Quinidine (Ia) just tells all the cells to STFU so it can reset the rhythm


Non-selective (Propanolol, Sotalol, Timolol)

Propanolol - use x Atrial Tachyarrhythmias

Bronchospasm, Hrt Failure, Bradycardia AV Block, Raynauds, Depression, Sex Dysfx: see above*: Sotalol may cause Torsades de Pointes

ISA (Acebutolol)

Class II - β Blockers are GREAT x Tachyarrhthmias

Class III K+ Blockers


Ibutilide use x A Fib/Flutter;

Dofetilide orally BID

Torsades de Pointes

Class IV Ca Antagonists (Nifedipine Is NOT an Antiarrhthmic agent)


Verapamil AV SA Dysfx, Asystole

Diltiazem

Not Nifedipine Not Nifedipine Not Nifedipine Not Nifedipine Not Nifedipine Not Nifedipine Not Nifedipine Not Nifedipine Not Nifedipine

Class V Cardiac Glycosides


Digoxin/Digitoxin?

Cardio-Selective (Atenolol, Metoprolol, Esmolol)

Atenolol DOC x something; ↓ automaticity by ↓ SAS; ↓ SAS related responsiveness of ischemic tissue; ↓ AV nodal conduction

Esmolol is new It looks like Ach, blocks the AV node and then is destroyed.

α & β blockers (Labetolol)


Amiodarone (also Ia Na channel blocker and Ca channel blocker)

Delays repolarization; marked ↑ in APDuration and ERP (effective refractory period)

Good x ischemic tissue and during V Tachy to slow down excitability Hz by ↑ prolonging AP duration

Pulmonary Fibrosis (fatal), Irreversible Liver damage, Constipation, bluish discoloration, thyroid dysfx (from I's) yellow discoloraton of eyes, Torsade de Pointes Fatal arrhthmias but these are rare. Life saving prop's far outweigh.

w β blocker → inhibition of both; w α blocker → ↓ conduction velocity in all cardiac tissue; ↑ Toxicity w Procaine

Has a 30 day half life (bad)

Torsades de Pointes; Prolongs QT interval when acting as K channel blocker

use x Atrial Tachyarrhythmias, A Fib;

Torsades de Pointes, Prolongs QT interval

Sotalol (oooh also a β blocker)

use x Atrial Tachyarrhythmias


↓ SA automaticity; ↓ AV nodal conduction velocity


Don't use w Propranolol or Disopyramide

↓ SA automaticity; ↓ AV nodal conduction velocity


↓ SA automaticity; ↑ ventricular Delayed After Depolarization (DAD); ↑ Excitability bc depolarize membr pot; Toxic doses have adverse effect.; Conduction velocity ↑ in atria, ↓ in AV node, ↓ in ventricles at toxic doses


SA Bradycardia, SVT, AV Block, Jxal Tachycardia, V Tach, V Fib (20% of pts have SDFX)

Tx toxicity w K (to lvl @ 5 mEq/dL), Lidocaine to hyperpolarize, Dig Fab Fragments, DO NOTUSE PADDLES, VERAPAMIL or BRETYLIUM

Adenosine DOC x PVST Heart Transplant

Atrial Tachyarrhythmias - Tx w Propanolol, Dofetilide, Sotalol, Digoxin or Verapamil

Wolf Parkinson White (WPW) Syndrome (a ventricular pre excitation thing) - ↓ AV Node via Vagal Maneuvers, Verapamil Digoxin, Propranolol; ↓ Accessory (kent bundle) w Amiodarone QPD Flecanide Propanlolol

Torsades de Pointes - Stabilize w MgSO4 (DOC) remove causative agents (eg quinidine, amiodarone), give K to ↑ serum K lvls to 5+/- .5mEq/L

Paroxysmal Ventricular Tacnycardia (PVST) - DOC is Adenosine

↓ cAMP, ↑ gK, ↓ automaticity of SA node; Conduction velocity ↑ in atria (vagomimetic), ↓ in AV node

Flushing, SOB, Bronchospasm, HA, Hypotension, Nausea, Paraesthesia

SVT - DOC=Adenosine (but may cause asthma attack) Vagal Maneuvers, Digoxin, Phenylephrine (↑ TPR → ↑ vagal RE), β blockers, Verapamil (IV): Prophylaxis via Verapamil, β blocker (NOT Esmolol) AVOID CAFFIENE CIGARETTES

V Tach - tx w Lidocaine (↓ V automaticity, Rapid depolarization in nml, Bidirectional block in Ischemic), Procainamide (↓ phase 0, ↑ ADP, ↑ ERP, ↓ V automaticity), Propranolol, Bretylium (↑ ADP, ↑ ERP) DC Cardioeversion (the paddles)::: None of these incr survival. HA!

Beta Lactam AntibioticsPenicillins

Name Class Spectrum MOA DOC Toxicities/SDFX Metabolism Contraindications Resistance Administration

GENERALLY Staph Strep??

Penicillin APenicillin F

Penicillin G

Penicillin V penicillinase penicillinase oral

Methicillin not used all too much staph aureus Nephrotoxic oral

Ampicillin shigella oral

Carbenicillin (pseuodmonas, proteus) poor absorption injection

Oxacillin oral

Nafcillin injection

Cloxacillin

Dicloxacillin

Amoxicillin

Bacampicillin Metabolized to Ampicillin Oral

Derivative of carbenicillin klebsiella

Ticarcillin Pseudomonas klebsiella

Azlocillin klebsiella

Mezlocillin/Pipercillin

D Penicillamine Chelates Copper Wilsons Disease

Drug Drug Interactions or Combos

cell wall synthesis inhibitor @ transpeptidase enzx; activation of autolytic enzx

Anaphylaxis (immediate, accelerated, delayed), epilepsy, nephritis, hematuria, hemolytic anemia (rare), GI, incr Na+

Oral contraceptives lose activity if + PNC b/c gut bact activate BCPs; lose activity if + TTCCL

excreted in the urine; picks up protein at lactam ring creating a hapten leading to allergic rxn

no metabolism, drug destroying, drug can't penetrate, mutation, bioch indux, conjgx, transdx, transposition

Narrow Spectrum G+

combine w Probenicid (weak acid) to compete for excretion; Add procain (charged) to decrease absorption and incr T1/2; add phenoxyacetic acid to make acid stable and thus available orally

short T1/2 (<60 mins), renal excretion

injection b/c not acid stable

Narrow Spectrum G+

Narrow Spectrum

B lactamase resistant :-); staph aureus…damn

created to overcome the Narrow Spectr of PNC G

Broad Spectrum

Ampcl+Sulbactam (B lactamx inhibtr) x incr efficacy; BCP lose contraceptive activity w Ampcln

penicillinase; NOT active vs Klebsiella or Pseudomonas

created to overcome the Narrow Spectr of PNC G. Not much used anymore

Broad Spectrum

loses activity if + gentamycin b/c chem rxn so give staggered

Given w Na so watch Na levels

penicillinase; NOT active vs Klebsiella or Pseudomonas

Staph aureus starting to become resistant

Narrow Spectrum

B lactamase resistant :-)


Narrow Spectrum



Narrow Spectrum



Narrow Spectrum


Amox+Clavulinic acid (B lactamx inhibtr) x incr efficacy

oral (better vs Ampicillin)

prodrug (ampicilin is active compound

Geocillin (Carbenicillin Inodyl)

Narrow Spectrum, G-

Pseudomonas (best vs Psuedomonas of PNCs), G-

Pseudomonas AND klebsiella G-

Not an Antibacterial

D-Cycloserine (2ry tx of TB (1 of 4))

Cephalosporins


GENERALLY excreted in the urine cross rxn w PNC allergy oral?

Cephalothin 1st Genertion G+ (staph endocarditis) IM/IV

Cefazolin 1st Genertion G+ (E. coli, Klebsiella) IM/IV

Cephalexin 1st Genertion G+ (klebsiella) oral

Cefadroxil 1st Genertion G+ (UTI) oral

Cefamandole 2nd Generation (ear infx, sinusitis) IM/IV

Cefoxitin 2nd Generation (anaerobes) IM/IV

Cefaclor 2nd Generation oral

Cefuroxime 2nd Generation (meningitis)

Cefotaxime 3rd Generation oral

Ceftizoxime 3rd Generation oral

Ceftriaxone 3rd Generation

Cefixime 3rd Generation oral

Cefpodoxime Proxetil 3rd Generation oral

Cefepime 4th Generation (pseudomonas)

Cefpirome 4th Generation (pseudomonas)

Other Beta Lactam Drugs


Carbapenem Imipenem

does not need inhibitor

disrupts erasamase at stage 2 of cell wall synths; erasamase converts L-alanine to D-alanine so it disrupts the bact cell wall synths


Broad Spectrum

same as PNC, cell wall synths inhibition, auto lysis induction, and …

(proteus, E. coli, klebsiella)

More toxic vs PNC esp 1st gx; irritation at IM inj site; thrombophlebitis @ IV; hypersensitivity; superinfx;

Synergistic w other nephrotoxc drugs

less susceptible to B lactamase vs PNC

Nephrotoxic synergistic w AG

Broad Spectrum G+ some G-

MTT causes bleeding. GIVE W VITAMIN K; disulfram reaction

alternative if allergic to ampicillin or amoxicillin







Broad Spectrum more G-

Cross BBB (good if you have CNS infections)









Broad Spectrum Good G-


Broad Spectrum Good G-



Broad Spectrum - anaerobes

(anaerobes, UTI, LRI, GI, Gyn infxs)

must give w cilastatin to inhibit kidny metabolism

kidney enzx inactivates so must give w inhibitor

Carbapanem Meropenem

Broad Spectrum - anaerobes

(anaerobes, UTI, GI, Gyn infxs)

Monobactam superinfx may occur lactamase resistant :-)

Vancomycin G+

Bacitracin cell wall synthesis inhibitor

Polymixin B G- infx Nephrotoxic if given IV topica (ophthalmic/otic)

Colistin Sulfate G- infx

AntiFolates

Sulfonamides


GENERALLY pills, orally, cheap :D

sulfasalazine

Methotrexate large molec antifolate cancer

Small Molec Antifolates thymine derivatives (malaria) prodrug incr folate reductase

Prontosil Sulfonamide prodrug

Bactrim (Septra) AIDS

G- rods ONLY

NO PNC cross hypersensitivity :-)

Beta Lactamase Inhibitors (Clavulanic acid, Sulbactam, Tazobactam)

inhibit beta lactamase (no antibacterial activity by themselves)

Clavulanic Acid + Ticarcillin or Amoxicillin; Sulbactam + Ampacillin; Tazovactam + Pipercillin/Mezclocillin (combos needed x activity)

cell wall sythesis inhibtr via binding D-ala D-ala

(staph aureus, C. diff, commonly used x PNC resistant drugs)

Red Man SSx, (hives, HoTN, flushing, rush, chest pain); ototoxic, injx site irritation,, rash, chest pain, hypotension, synergistic w Nephrotoxic drugs (AG)

AG + vanc = Synergistic Nephrotoxicity

Bact chg the D-ala D-ala so drug has nowhere to bind

IV (IM) via slow infusion to avoid Red Man SSx, oral x gut bact (e.g C. diff)

(staph infx that don't RE to PNC meth, oxa naf or cloxacillins)

Nephrotoxic if given IV (less so if given orally)

Synergistic w other nephrotoxc drugs

topical intrathecal/pleural (IV/IM)

detergent, cell membr disruption

detergent, cell membr disruption

Circumoral paresthesias if IV, nephrotoxic


Broad Spec (G+ cocci, G- cocci/rods

compeltes with paba for coupling enzyme so bact can't make vit. B9. free drug is active drug; pH dependant (will crystalize out at low pH so drink lots of water

none but alt x (UTI, nocardiosis, shigella, trachoma, chlamydia, pneumocystis jirovechi)

StvJonSSx (from long lasting sulf Rx), decr vit K synth(by wiping out gut bact), hypoglycemia/GI, hepatitis, crytalluria, CNS-rare-,

incr warfarin activty (wfn is bumped off plasma prot by sulfmds causing unwanted bleeding); hydantoin (same as wfn but is an anticonvulsant), incr T1/2 Phenytoin (competes x micrsomal enzx),

good distribution, bound to plasma prot making it difficult to metabolize, renal excretion (unchanged), acetylation in liver loses activity but retains toxicity, T1/2 depends on kidny fx

gluc6phos DH defx (NADPH is depleted and can't reduce G6PDH-causes hemolytic anemia), AIDS, kernicterus (new borns; bumps off bilirubin and causes mental retardation), allergic to SO2 (e.g. Celexa)

decreased permeability, coupling enzyme changes, paba prodx incr.

5aminocyclocyclic acid is cleaved off (active part)

Reum. Arth, colitis

Inhibit folate synths (Folate to FH2; or FH2 to THF4) | Cancer-MTX forms complx w polyglutamate and is trapped inside cell to incr activity

Acute Lymph Leuk, choriocarcinoma, Burkitts lymphoma, Psoriasis, immunosuppres (x organ transplants). TOO TOXIC x antibact

GI ulcers, bone marrow depression, hepatic toxicity, HA, pulmonary, renal, pseudolymphoma. (Tx x toxicity = Folinic acid or folic acid)

pregnant fem, fem trying to get preg.

treat toxicites w folinic acid (cancer) or folic acid (psoriasis RA); IM, IV, IT

Depends on R1, R2

Inhibit folate synths (Folate to FH2; or FH2 to THF4) Thymine Derivative, some are prodrugs

StvJonSSx, hypersensitivity, GI, megaloblastic anemia, N/V, anemia, incr serum creatinine

sulfa w trimethoprim (UTI, prostatitis, otitis med, chronic bronchitis, pneumocystis jirovechi (not AIDS pts) shigellosis, toxoplasmosis

metablized to sulfanilamide (active cmpd)

Slufamethoxazole/Trimethoprim combo

UTI, prostatitis,otitis media, shigella, toxoplasmosis

incr [creatine], StvJonSSX, displaces drugs bound to plasma prot causing incr lvls e.g. warfarin

Pyrimethamine small molecule antifolate synergism w sulfa drugs oral

Trimethoprim small molecule antifolate NVD synergism w sulfa drugs prodrug oral

DNA Synthesis InhibitorsQuinilones


GENERALLY

Nalidixic Acid

Cinozacin

Fluoroquinilones


GENERALLY

Ciprofloxacin ANTHRAX NVD, HA, abnml LFTs,

Levaquin/Levafloxacin NVD, HA, abnml LFTs,

Norfloxacin

Ofloxacin

Nitrofurantoin unk UTI RARE-liver, lung, GI, skin pts w severe renal insfx

plasmodia, sporozites

inhibit dihydrofolate reductase inhibiting folate synths

suppression of chlorq resist falciparum sp usu in combo w other TB mx

b9 defx, macrocytic normochromic anemia, megaloblastic bone marrow; leukopenia, granulocytopenia rare StvJonSSX



DNA gyrase - topoisomerase II (G-) or IV (G+)

(STD, UTI, GI infx, URI, SSTI, bone/joint infx {better vs sulfa}, TB, mycobacterium avium cmplx)


(STD, UTI, GI infx, URI, SSTI, bone/joint infx {better vs sulfa}, TB, mycobacterium avium cmplx)



STD, TB (2ry), SSTI, mycobacterium infx; better than sulfa drugs

GI, cartilege growth inhibition (in children), cardiac arrythmias, crystalluria (drink lots of water)

Liver metabzd, Excreted in urine/bile (depends on

which) acid pH decr activity, rapidly absorbed,

children, preg Fem better than sulfa drugs


Liver metabzd, Excreted in urine/bile (depends on

which) acid pH decr activity, rapidly absorbed,

children, preg Fem


children, preg Fem



NOT a quinolone, but damages DNA.

Protein Synthesis Inhibitors


GENERALLY depends on geography conjugation oral

Erythromycin Macrolides Liver/kidney damage

Clarithromycin Macrolides

Azithromycin Macrolides

Lincosamides antagonize macrolides oral (w/ food?)

Clindamycin Lincosamides oral (w or w/o food :-)

Tetracycline Tetracycline

Minocycline Tetracycline Lyme teeth discoloration not good for UTIs


G+, G-, Broad Spectrum

stop ribosomal complex from moving, disrupt aa binding

G+, Bacteriostatic (cidal @ high doses but w toxicities

Binds to 50S ribosomal subunit, inhibits translocation step and inhibsc cmplx formation

Mycoplasma pneumonia, Legionella, Diphtheria, also used to tx bacterial bronchitis, otitis media, acne(topical). Prophylax endocarditis colon/oral surgx [2ry Staph Strep, tetanus, chlamydia, lyme; some G- N. Meningitidis, H. flu, B. pertussis]

estolate form - cholestatic hepatitis (GI pain, hepatomegaly, incr bilirubin, eosinophlia; reversible); free (active) form- N/V/D

ERTHX + Clindamycin is antagonistic; ERTHX + PNC = syng renal damage; decr cytochrome P450 activity so other Rx/herbs have more activity Chloramphenicol+Erythromycin=antagonism by 50S competition

concentrated in the liver, bile excretion

Induced resistance, 50S ribosome mutation, efflux pumps, hydrolysis/destrx of Rx; cross resistance to other macrolides and clindamycin

must coat tablet to protect it from stomach pH, so it dissolves in duodenum; good body distr

Broad Specturm


H. flu, mycobacterium avium (AIDS pts usu), H. pylori

decr cytochrome P450 activity so other Rx/herbs have more activity

Broad Specturm


(mycobacterium avium, Toxoplasmosis encephalitis, chlamydia urethritis) Erythromycin 1st

Lincomycin (not used anymore) Broad

Specturm

50S inhibition, translocation inhibition

too toxic to use, 50S inhibition, blocks translocation step

G+, Bacteriostatic (cidal @ high doses but w toxicities

50S inhibition, translocation inhibition

anaerobic infx (bacterioides fragiles), strep pyogenes, diplo pneumoniae, staph aureus; 2ry choice if allergic to PNC

Pseudomembaranous enterocolitis (can be fatal so change to vancomycin)

antagonize macrolides/erythromycin

metabzd in liver, excreted by kidneys

cross resistance w erithromycin, ribosomal mutations

Broad Specturm G+, G-

30S inhibition previnting t-aminoacyl binding; inhibits fMet tRNA from binding

Brucella Bacteroides (Lyme, spirochetes, mycoplasmas amebae, cholera, STDs); SIADH

GI (staph enteritis could cause superinfx), hypersstvy, photosenstvy, liver damage, renal damage, dizzy/vertgo, damage to teeth/bones causes discolored teeth

Chelates heavy metals (Ca, Mg…) which reduces absorption; TTCCL decreases activity of BCPs via killing gut bact needed for BCP activation; PNC+TTCL=antagonistic

Lower dose if kidney disfx. Excretion depends on GFR (except for minocycline and doxycycline); kids <10 preg fem

Gradual reisistance via R factor and efflux, overuse. Cross resistance w streptomycin, erythromycin, ampicillin, chloramphenicol, oxacillin, and cephalosporins. G- usu have cross resistance w chloramphenicol (not G+)

oral not so good absorption, IM/IV


30S inhibition previnting t-aminoacyl binding

oral not so good absorption, IM/IV

Doxycycline Tetracycline Lyme teeth discoloration oral good absorption

Tetracycline ssti, intra-abdominal infx GI, N/V/D IV ONLY

Chlorapmphenicol lower dose if liver disease oral

Aminoglycosides


GENERALLY Aminoglycosides

Streptomycin Aminoglycosides TB (must combo); plague mutation of 30S subU IM (no CSF distribution)

Kanamycin 2ry TB

Neomycin Aminoglycosides

Tobramycin Aminoglycosides bacteremiaParommycin Aminoglycosides

Gentamicin Aminoglycosides G- Renal excretion via GFR



not good for UTIs; Carbamazepine + doxy = decr doxy lvls via induction; PHB + doxy = decr levels via induction; PHT + doxy = ditto;

Tigecycline (not important)



Do NOT use to tx Proteus/Pseudomonas

Broad Spectrum

prevents 50S from binding to mRNA, inhibits peptidyltransferase (also inhibits euka cells w diff mechanism)

Salmonella typhosa (rickettsia, mycoplasma, lymphogranuloma). NOT USED FOR TRIVIAL INFX

superinfx, hypersensitivity, irreversible delayed aplastic anemia Gray Baby SSx (renal damage, cardiac collapse), good diffusion to CNS, and inner eye (good thing), pancytopenia (rare/severe), GI, neuro sdfx, superinfx,

not good w TTCCL, Polymyxin B, vancomycin, hydrocortisone b/c of antagoinism; Chloramph+Erythromycin=antagonism by 50S competition

liver glucuronidation or hydroxylation inactivates, inactive drug excreted by kidny, incr plasma lvls if liver disfxing

R factor transmits gene x acetylation


Narrow Spectrum G-

prot synths inhibition; cell membr damage via; binds to 30S ribosome

(G- rods causing meningitis)

CN VIII damage, renal damage allergic dermatitis (topical), neuromuscular jx blocker, vertigo, dysmetria, +Romberg sign

ototoxicy if +Ethacrynic acid

unchgd excreted form by kidny via GFR; short T1/2, low TI, dosing schedule is tricky so instead of lots of small doses Rx is a few heavy doses instead of lots of small doses

renal disfx incr plasma lvls so lower dose; synergistic renal tox w other renal toxic drugs

resistance via R factor transfor; mutation of 30S subU; adenylation in kanamycin streptomycin, gentamycin, tobramycin; phosphorylation in kanamycin, streptomycin; acetylation in kanamycin, neomycin, tobramycin, amikacin, gentamycin strreptoycin

IM, subQ, oral (x gut infx; bad absorption in gut), intrathecal, topical

inhibits fMet binding; inhibits translocation step (aminoacyl binding to tRNA); require O2 for transport thru cell walll

vestibular system disruption, hearing loss if high doses, peripheral neuritis, facial paresthesia, NMJ blocked in high doses, rash/hives, kidny damage

Must combo w other TB drugs; strpmcn + PNC to tx enterococci; DO NOT GIVE ALONE b/c resistance develops quickly; synergistic activity w Erhthromycin to tx Strep faecalis endocarditis

Broad Spectrum

E. coli, Proteus, Shigellae,, Klebsiella; prophylactic x bowel surgx (staph enterocolitis)

Nephrotoxic ototoxic, contact dermatits

NOT effective x Pseudomonas or Bacterioides

topical oral x gut infx,

Pseudomonas resistant to Polymyxin B(Klebsiella, Proteus , G- rods causing meningitis; E. coli, ); Plague

Nephrotoxic, vestibular ototocicity, CNS toxicities

Genta + Carbenicillin = decr genta activity via chemical rxn; Genta + Cephalothin = synergistic nephrotoxicity via tubular necrosis; Genta + Polymyxin B = synerg nephrotoxicity and NMJ block; Genta + Kanamycin = synerg ototoxic effects;

intrathecal (CNS toxicities)

Viomycin Aminoglycosides 2ry choice x TB arises quickly

Spectinomycin Aminocyclotol 30S subU inhibitor IMgonorrhea in urethra, prostate or cervix if N. gonorrhea is susceptible

pain at injx site, hives, N/V, insomnia, dissiness; rare-renal/liver damage, incr BUN, decr clearance, incr LFTs

pts sensitive to PNC usu tolerate spectomycin

Ineffective in extragenital gonorrhea/syhp

Streptogramins

Quinupristin streptogramin G+ 50S inhibitor combo drug w Dalopristin oral

Linezolid Oxazoladinone G+ GI, HA, MAOI inhibition poor people

Netilmycin Oxazoladinone

Antifungal Drugs


Polyenes

Nystatin Polyene N/A

Amphtericin B Polyene N/A

Imidazoles/Triazoles

Ketoconazole

VR E. faecium, bactremia, URI caused by MRStaph/Strep PNC resistant Strep pneumoniae

joint muscle pain, decr cytoP450

R factor transmits binding site mutation

multi-drug resistant organisms


yeasts and fungi

binding to ergsterol causes cell membrane leakage

Candida albicans; Moniliasis (oral or topical) (Cryptococcus, Histoplasma, Blastomyces, Trichophytion, Epidermophyton, Microsporum; sometimes mycoplasma bact),

none unless given systemically (oral - mild N/V, diarrhea; IV - hemolytic anemia, kidny damage)

topical, oral (excreted in feces) vaginal tablets,

.3 mg <MIC< 1 mg. Dose is 2x MIC that lab gives you.

binding to sterol causes cell membrane leakage

severe deep fungal infx (e.g. meningitis, bone, pnemonia…); topical

VERY TOXIC: NEPHROTOXIC, hypersensitivity, chills, fever, phlebitis, HA, anemia, anorexia, decr renal fx HoTN, hepatic failur, jaundice, hepatocullular disfx,

Use only in hospital w fatally ill pts and make sure pt is "healthy" enough to take th Rx. Daily dose not to exceed 1.5 mg/kg; AmphoB allows Rifampicin (usu bact Rx) to penetrate fungal cell wall and kill fungi, but is toxic to host); intrathecal administration causes chemical meningits

DO NOT EXCEED 4g else renal damage, do LFT's, renal fx test b/f tx

topical, IV (low doses long time, .5mg/kg)

Broad Spectrum

Inhibition of ergosterol syths causing membr disruption

systemic infx (coccidiomycosis, paracoccidiomycosis, histoplasmosis-formally txd w Amph B

inhibits cytchrP450 (disrupts steroid hormone metbz and other drug metabz), elevates LFT's

Keto + antacids decr keto activity b/c keto needs acid environment to be soluable/active; keto + cyclosporine incr cyclosp lvls; keto decr steroid metablzm

topical, oral (being replaced by itraconazole and vriconazole; voricon does not inhibit P450 as much which is good for polypharmacy)

5-Flucytosine prodrug oral (good absorption)

Griseofulvin fungastatic N/A

Miconazole

Fluconazole Resistance


Undecylenic Acid Fatty acid? ??? GI topical

Tolnaftate Fatty acid? Trichophyton rubrum GI topical

Terbinafine Allylamine oral, topical

Caspofungin Echinocandin Aspergillosis nyeh, GI, incr LFT

Anti TB Drugs


Candida albicans (Cryptococcus, Torulopsis, Aspergillus)

Deaminated to 5fluoracil (active cmpd) which replaces U in mRNA resulting in screwy peptides. Also converted to 5fluorodeoxyriboseMonoPhos. Which inhibits thymidylate synthase. Basically commits suicide

Candida albicans (Cryptococcus)

Fatal Bone Marrow Depression, diarrhea, AIDS pts have trouble tolerating

Usefulness lmtd b/c cytopls membr not permeable to 5Flu, so AmphoB potentiates 5-flu effectiveness (tx x Candida & cryptococcus infx)

HIGH lots of things become resistant

binds to cell membr, kills(?) growing fungi by disrupting mitotic spindle. Binds to host keratin creating an environment where fungi can't grow and the fungi is shed w natural shedding process

skin and nail infx, athletes foot. (Microsporum, trichophyton, Epidermophyton; athletes foot and stuff): (systemic x candida albicans)

mild; HA (gone in a few days), memory probs, GI

Gris + PHB decr Gris lvls by decr absorption; Gris + warfarin decr warfarin activity by induction; Gris induces prophyrin synths causing porphyria attack to those pts w porphyrias

oral (good absorption if eaten w fats), IV. Up to 12 mos to treat dermatophytes

Broad Spectrum


Tinea pedis, cruris, vesicolor (vulvovaginal candidasis) coccidiomycosis

systemic - arrythmias, phlebitis, HA

synergistic with coumadin (anticoagulate), use if AmphoB not an option

low vit K, pts taking anticoagulants

topical, not given systemically


oral/esophogeal candidiasis in AIDS pts (cryptococcal meningitis; prevent relapse after Amph B)

GI, vomiting. In AIDS pts - StvJon SSx, liver damage, thrombocytopenia, rash)

give antiemetic to counteract vomiting; phenytoin lvls incr; anticoagulant lvls incr if + flucon

teratogenic (don't give to preg fem)


Tinea pedis, cruris, vesicolor, ringworm

Squalene epoxidase inhibitor (ergosterol syths inhibition)

fungicide by squalene buildup

Squalene epoxidase inhibitor (ergosterol syths inhibition)

Trichophyton, Epidermophyton, Microsporum (aspergillus, candida, sporothrix schenckii, malassezia furfur)

HA, diarrhea, dyspepsia, abd pain; chg in tast patterns; incr LFT (severe hepatotoxicity rare)

T1/2=16 days, liver metabolizes, inactive cmpd excreted in feces kidny

Inhibits beta 1-3 glucan syths

Aspergillosis after AmphoB has failed


Streptomycin Aminoglycosides 1ry for all TB tx: oral;

Cycloserine 2ry must be given w B6

Ethionamide GI, HoTN, liver toxicitiesLevofloxacinViomycin AG 2ry prot syths inhibitor 2ry TB ototoxicityKanamycin AG 2ry prot syths inhibitor 2ry TB ototoxic nephrotoxicAmikacin AG

Rifabutin/Rifampin 1ry induces P450 from RNA pol mutation

Capreomycin peptide

Aminosalicyclic acid folic acid synths

Ciprofloxacin

Isoniazid TB combo

Ethambutol excreted in urine/feces DO NOT use in kids oral

inhibits fMet binding; inhibits translocation step (aminoacyl binding to tRNA); require O2 for transport thru cell walll

Ototoxicity, nephrotoxicity (all AG do)

INH + Rifampin + Pyraz + Ehambutol or Streptomycin is standard 4 Rx tx. use INH + Rifampin + pyrazinamide (lose pyr after 2 mos); INH +Rifam+Ethambutol is safe x preg fem

Start to see improvement of morbidity in 2 weeks

Seizures (esp if predisposed), peripheral neuorapothy

ppl w seizures, depression (exacerbated)

inhibits RNA polymease (initiation step)

TB combo, active systemic TB, TB mingitis,eradication of meningiococcal carrier state; Mycobacterium avium

reare hepatitis, turns host fluids orange, flu like ssx

must combo; maybe can use AmphoB to let rifampin into fungal infx; Rifampin + AminosAcid block the absorption of the other from gut (bad thing); INH + Rifampin + Pyraz + Ehambutol or Streptomycin is standard 4 Rx tx. use INH + Rifampin + pyrazinamide (lose pyr after 2 mos); INH +Rifam+Ethambutol is safe x preg fem

INH+Rifampin have additive liver toxicity <-toxicity; causes loss of BCP activity

2ry agent when 1ry no longer useful

ototoxicity, renal toxicity (not as bad as AG)

2ry b/c of GI probs

bad diarrhea b/c of high dose (8g)

Rifampin + AminosAcid block the absorption of the other from gut (bad thing); BCPs lose effectiveness; induction of liver;

requires 8g per day

1ry TB tx, NO G-/+ activity

isonicotinic acid uses up causing OH buildup in cell; interferes w mycolic acid synths causing cell wall damage

INH metabolit causes toxicity B6 defx, peripheral neuropathy; liver toxicity esp w EtOH (death); szr if prone;

INH + Rifampin + Pyraz + Ehambutol or Streptomycin is standard 4 Rx tx. use INH + Rifampin + pyrazinamide (lose pyr after 2 mos); INH +Rifam+Ethambutol is safe x preg fem; give w B6; INH inhibits metbz of Phenytoin

prodrug (active cmpd is converted by catalase to isonicotinic acid); LONG T1/2 you can give; acetylation inactivates; P450 metabolism

Treat <20yos. DO NOT TREAT if >35yos

mutation of catalase TB has high mutation rate so selectivity is common :(

oral good absorption; prophylaxis x 9 mos if evidence of expossed (only prophylaxic tx

1ry TB tx, NO G-/+ activity

mycolic acid inhibition ro RNA syths inhibtion

TB combo, mycobacterium avium cmplx

retrobulbar neuritis @ high doses (decr visual acuity, red green color blindness)


Pyrazinamide 1ry reinfection

Dapsone Leprosy use 3-4 leprosy mx to startClofazimine Leprosy use 3-4 leprosy mx to startAmithiozone Leprosy use 3-4 leprosy mx to start

Thalidomide Leprosy teratogen use 3-4 leprosy mx to start

Ethionamide 2ry Leprosy use 3-4 leprosy mx to start

AntiViral Drugs


Blocks binding to cell decr dose in geratric pts

prodrug teratogenic, carcinogenic,

Vidarabine purine

Interferon alpha must be taken for 1 yr

Acyclovir purine prodrug

GanciclovirRibavirinCidofovirTrifluridineFoscarnet

HIV Drugs- 1PI + Ritonavir + 2NRTI (specific combo) = 4 drug Tx; or NRTI (combo)+ NNRTI = 3 Drug Tx

Liver Toxicity TOXICITY MANDATES hospitalization


HIGH if tx w/o other drugs

pregnant women (day 20-50 cuases seal limbs in fetus)


Amantadine and Rimantadine (better mx)

prophylactic tx of Flu A2 in elderly (parkinson)

nervousness, depression, epilepsy esp if prone to psychosis

do not use w bactrim, antihistamines (causes neurotoxicity; esp in older ppl, hmmm)

NOT USED CURRENTLY B/C OF RESISTANCE IN ALL STRAINS OF FLU

decr dose in elderly b/c of decr renal fx

Idoxuridine (historical significance only)

antimetabolite; DNA synths inhibitor by stopping DNA elongation; incorporated into DNA causing DNA breakage, muation rate incr; selectivity due to rapid rate of virus replication

(herpes keratitis from herpes type I, if nothing else left)

photosensitivity, edema causing lacrimal duct occlusion; slows down healing process

topical, (systemic-HARDLY)

(DNA viruses via decr synthesis)

replaces adening to stop DNA synths

(herpes keratitis from herpes type I, if idoxuridine not available); chicken pox, herpes encephalitis via systemic; ocular herpes infx

at high doses stops host DNA synths (polymerase); carcinogen, teratogen, mutagen

systemic - allopurinol + vida causes decr activity of gout mx

deamination causes inactivity; prodrug

topical, (systemic-HARDLY); acyclovir is better

inhibit virus binding by binding to virus; inhibit at all steps of virus rep

Chronic Hepatitis (B, C) (Karposis sarcoma, melanoma)

neurotoxic, flu like ssx usu resolves in days, bone marrow suppresion, exacerbate depression/suicide

inhibits viral DNA polymerase; syths inhibition

Herpes (all kinds and manifestations)

inactivated if taken w allopurinol

Zidovudine NRTI @ low lvls or monothpy

Lamivudine NRTI @ low lvls or monothpy

Emtricitabine NRTI @ low lvls or monothpy

Tenofovir NRTI NOT prodrug @ low lvls or monothpy

Efavirenz NNRTI HIV @ all stages; teratogen cytP450 indux preg fem, liver disfx @ low lvls or monothpy

Atazanavir Protease inhibitor

Fosamprenavir Protease inhibitor

Lopinavir Protease inhibitor

Ritonavir Protease inhibitor inhibits cytP450

Enfuvirtide Fusion inhibitor; peptide binds to gp41 HIV @ all stages don't give if allergic injx

AntiParasitic DrugsAntiMalarial


GENERALLY

Chloroquine Aminoquinolone

incorporation into DNA causing early DNA termination and slow replx by blocking reverse transcriptase

HIV @ all stages; prophylaxis x exposure and newborn

damage tissue that are constantly turning over via mt toxicity; lactose acidosis, liver failure low platelets

combo Lamivudine+Zidovudine

prodrug concerted to nucleotide




combo Lamivudine+Zidovudine





combo Tenofovir + Emricitabine




damage tissue that are constantly turning over via mt toxicity; lactose acidosis, liver failure low platelets, renal insfx

combo Tenofovir + Emricitabine

nonompetetive inhibitor of reverse transcriptase

inhibit final prot metabz of HIV prot


long lasting DM, hyperlipidemia, diarrhea

combo w low dose Ritonavir, then combo w NRTI

@ low lvls or monothpy; cross resistance













long lasting DM, hyperlipidemia, diarrhea inhibits cytP450

combo b/c incr T1/2 of other drugs; but contraindicated if pt taking other mx


painful injx; incr chance of bact pneumonia



sulfa drugs, trimethoprim, quinolones

DNA replication disruption; B9 syths inhibition

Binding to DNA inhibits nucleic acid synths

use during erythrocytic phase of maria cycle; schizonticide;

GI, HA, malaise, vertigo, blurry vision.

Coadministration w Primaquine is required to tx /prevent relapse;

Excreted in tears absorbed by corneal epithlm causing edema and opacifications of cornea (retinal aa constrx causes retinal ischemia and visual impairment)

if Plasmodium sp can't concentrate in cell then mx won't work; falciparum is chloroquine resistant and reqs cinchona and anti-folates

as prophylactic tx must be given x 6 mos straight after leaving endemic area.; as suppressive therapy 2.5 g orally w/in 3 days, IM if necessary;

Mefloquine

Hydroxychloroquine

Quinine Cinchona alkaloid

Primaquine 8-Aminoquinolone ppl w Gluc 6 P DH defx

Chloroquanide

Pyrimethamine

Trimethoprim

ppl w Gluc 6 P DH defx

Sulfa

Amebicides, AntiProtozoal Drugs


Metronidazole teratogenic

Diloxanide furoate

blood schizonticide

blood schizonts of P falciparum, vivax, Prophylactic ovale, malariae

interference with w fine coordination and spatial discrimination

not active vs P falciparum; pts w epilepsy or on psychiatric mx; pregn

prophylactic vs chloroquine resistant falciparum, ovale, vivax;

gamete of all Plasmodium sp EXCEPT falciparum

Binding to DNA inhibits nucleic acid synths

Chloroquine resistant falciparum sp

injx site irritation, retinal ischemia, hearing loss, ringing in ears, dizziness, N/V/D; Severe-blindness, deafness, vertigo, HoTN; thrombocytopenia, purpura, hemolytic anemia, agranulocytosis, blackwater fever (hemolysis, clotting, renal failure uremia, death)

usu given w anti-folates, pyrimethamine + sulfadiazine/dapsone (x choroq resist falciparum)

no resistance and we don't know why

IV/IM? as blood schizonticide; oral

tissue schizonticide; gametocidal

Exoerythrocytic P vivax and P ovale

well tolerated; acute hemolytic anemia

Chloroquine must be given w Prima for complete tx; + 4aminoquinolone x prophylaxis

no resistance and we don't want any



suppression of chlorq resist falciparum sp usu in combo w other mx

b9 defx, macrocytic normochromic anemia, megaloblastic bone marrow; leukopenia, granulocytopenia rare



suppression of chlorq resist falciparum sp usu in combo w other mx

b9 defx, macrocytic normochromic anemia, megaloblastic bone marrow; leukopenia, granulocytopenia rare

Diaminodiphenyl Sulfone (DDS)

Folic acid inhibition b/c it is a paba analog

GI, N/V/D, dermatitis, crystalluria, hematuria, hemolytic/aplastic anemia, granulocytopenia

Trimethoprim + Sulfamethoxazole (bactrim)

Bacrim+Amant=neurotoxicities in geriatric pts

pts taking amantadine, old pts


Iodoquinol

Emetine

Dehydroemetine

Chloroquine

Suramin Na

Melarsoprol

Na Stibogluconate

Pentamidine Isethionate

Nifurtimox

Quinacrine

Atovaquone


Piperazine Citrate

Thiabendazole

Mebendazole

Albendazole

Pyrantel PamoateParomomycinPraziquantelBithionolNiclosamideQuinacrine


Actinomycetes

General Features No Immune RE: b/c it's too far away. Reason for removal is usu. Cosmetic

Etiology Epidemiology Manifestations

Nocardia asteroides

Spirochetes

General Features Spiral shaped, Nonsporulating, Motile


Treponema pallidum

Actionmyces israeli, Propionibacterium propionicus, Actinomyces naeslundii

M>F 2:1, 15-35yo, usu after loss of nml flora

Actinomycosis-1)Cervicofacial-most common, usu follows dental caries and happens after trauma 2)Thoracic-pulmonary inf may be initiated by extentision or inspiration. Maybe spread to CNS 3)Abdominal-usus due to perforation of intestinal wall e.g. appdx rupture. ss(x) follow infd organ. 4)Genital-common in femms, usu w/ IUDs, ss(x) similar to PID, usu subclinical

75% of cases in Males unk reasons. 50% of cases to immunocompr, AIDS, EtOHics, cancer, chrnc pulmonary inf. Orgsms are wrdwde, soil and aquatic.

Nocardiosis-Pulmonary inf as transitory or chronic, rarely necrtizing, w/ many large abscesses. 2)May disseminate to organs w/ predilection to brain

M>F b/c of more exposure. Sub/tropical, Sudan, Mxco, usu soil dwellers.

Actinomycetoma-SubQ inf 1)Swollen lesion usu on foot/hand suppurating abscesses w/ grains (same as eumycetoma)

1)Modes of Inf-Passage through birth canal, infection in utero, contact during manifestation, blood transfusion 2)Adolescent to adults

Syphillis-1)Primary Stage-Hard chancre nonpainful (genitals-males cervix-fems) 2)Secondary Stage-Flu like ssx, skin lesions, mucous membrane lesions 3)Latent Period 4)Late Period/Tertiary Stage-Neurosyphilis:Asymptomatic or Symptomatic-Meningovascular, Parenchymatous (paresis, Tabes Dorsalis). Late Benign Syph-Gumma Formation

Teponema pertenue Children, Warm tropics

Treponema carateum Children, Warm arid tropics

Treponema syphillis Children, Arid subtropical

Reservoirs-animals (e.g. cows)

More Notes:

Oral MicrobiologyGeneral featuresEtiology Epidemiology Manifestations

Yaws-looks like warts on skin.

Pinta-Looks like skin is peeling, or becoming unpigmented

Bejel/Endemic-Mouth lesions, skin lesions, granulomatous lesions on skin nasophrx, bones

Borrelia recurrentis, hemsii, turicatae, parkerii

Relapsing Fever Tick Born (B. recurrentis)-More relapses but less severe. Louse born (B. hermsii, turicatae, parkerii)-Usu only one severe febrile episode

Borrelia burgdoferi, garinii, afzelii

Worldwide Reservoirs-Deer, mice Vector-ticks

Lyme Disease 1)Primary stg-erythema chronicum migrans 2)Secondary stg-rash, arthrits, neuro, cardiac 3)Tertiary stg-arthritis

Leptospira interrogans, biflexa

Leptospirosis-usu subclinical may cause fevers, conjuctivitis, Icterus jaundice Kidney/Liver dss

Bact of supragingiva is mostly G(+) sp. Bact of subgingiva is mostly G(-) sp. Disruption of these proportions → disease.

Streptococcus mutans, Lactobacillus acidophilus

Everybody everywhere is susceptible (babies falling asleep w/ bottle, ↓ salivary rate, late weaning). Brushing, Fluoride, Peridex (.12% chlorohexidine)etc etc. helps to prevent. ↑[L. acidophilus]≈[caries]. S. mutans main cause of oral infs.

Dental Caries-Decalcification of inorganic and organic portions of tooth via acids produced when bact act on CHOs

Legionella and BartonellaGeneral Features 1)Peru Ecuador, Colombia 2)G(-) rods fastidious (needs humidity w/ CO2) 3)Spread via sandfly Phlebotomus


Legionella pneumophilia

Bartonella bacilliformis

Bartonella quintana

Bartonella henselase

1)Microbial-brkdwn of epithelial wall provides entry, G(-) rods increase, tissue damage due to endotoxins of G(-) bact 2)Immunologial-allergic rxn of gingiva to mouthwash/toothpast, pemphigus vulgaris, lichen planus, neoplastic dss, carcinoma 3)Traumatic-blunt trauma, plaques, chemical (aspirin is caustic to epithelial tissue)

1)Periodontal Disease-Gingivitis, Periodontitis, Periodontosis, Periodontal Abscess, Drug induced gingival Hyperplasia, ANUG, Primary Herpetic stomatitis, Recurrent Herpetic Stomatitis, Herpetic Whitlow, Aphthous Ulcers, Candidiasis, Hairy Tongue, Dry Socket 2)Endodontic-Pulpitis

M>F 2:1, 50+yo, Summer, Smokers, EtOHics, immcomrsd, pulmo dss Spread via aerosol e.g. swamp coolers

1)Legionairres dss-Flu like ss(x) Fatal 2)Pontiac Fever-Flu-like ss(x) Self-limiting

1)Peru Ecuador, Colombia 2)G(-) rods fastidious (needs humidity w/ CO2) 3)Spread via sandfly Phlebotomus

1)Bartonellosis-Acute anemia → verruga Anemia caused by removal of infd sensitized RBC's, HA Myalgia. Anemic phase ends when humoral RE induced Chronic Bartonellosis w/ cutaneous lesions1-2cm for years

1)Spread via human louse Pediculus humanus

1)"Trench Fever"-Fevers at 5day intervals 2)Most commonly HA, xtrm wkns tibial pain Varies fr ass(x) to debilitating 3)Angiomatosis

1)Car Scrath Dss-Lymphadenopathy at site of inf 2)SBE 3)Bacillary Angiomatosis

Parasites


Entamoeba histolytica

Giardia lablia

Balantidum coli

Plasmodium falciparum

↓↓↓SubKingdom Protozoa↓↓↓

Reservoir: Only Humans thus human-human transmission only via fecal contaminated H2O w/ cysts. Flying bugs can transport feces cysts from feces to food Common in Tropics 1)Prot defx, Pregnant, immdfx Inf≠Dss, but may → assx carriers.

1)Amoebic Dysentery-abd pain, cramps, colitis w/ diarrhea→Bloody stools w/ 25poops/day. (R lobe of liver may be inf→rupture→lung inf. Length of illness days-yrs

WrdWde Childrn<10yo e.g. daycare centers Homosexual Males Reservoir:dogs, muskrats, sheep, lakes, rivers aka "backpackers dss" Transmission fecal-oral cyst is infective form Flying bugs can transport feces cysts from feces to food

1)Giardia-mild drrha to malabsorption syndrm, foul dirrha, abd cramps, farting, steatorrha Malnutrition b/c G. lamblia absorbs fat sol. stuff like beta carotene, B12 exacerbating malabsorption syndrm

WrdWde, Fem Mosquito is vector. Mosqo ingests diff sex sp., male matures to magetes female into macrogamete, fertilization forming zygote/ookineate/oocyst, oocyst turns to haploid sporozites, sporozites goto mosqo saliva glands, inf humans. In humans sporozites goto hepatocytes to become merozoites, release, inf RBC's, mature into trophozoites, merozoites, rupture, release more merozoites

1)Malaria-Early flu-like ss(x), Nausea, vomiting drrha, HA fever convulsions, joint pain

Toxoplasma gondii

Trypanosoma cruzi

Africa Tse Tse fly is vector 1)African Sleeping Sickness

More Notes↓↓↓SubKingdom Metazoa↓↓↓

General FeaturesEtiology Epidemiology Manifestations

Ascaris lumbricoides

Enterobius vermicularis

Stronyloides stercoralis

Wucheria bancrofti

Phylum Platyhelminthes Class ↓↓Trematodes↓↓ General Features Nutrient uptake via absorption Nonsegmented


Coccidian parasite, Cat is vector and reservoir. Immcprsd and pregnant are at risk. Cat eats cyst, cyst turns into trophozit, trophozit turns to oocyst, cat poops, humans ingest oocyst, oocyst turns into sporozit, inf and dss

1)Toxoplasmosis-Acute:chills, fever, HA fatigue, lmphadenitis, myalgia Chronic:rash, encephlitis, myocarditis

Children under 5, Americas Kissing bug is vector, inf but poops on human skin causing irritation, human scratches inf into skin, inf. Trypomastigotes invade phagocytic cells, develp into amastigotes, multiply, ruputure, mature to trypomastigit form, inf new RBC's (get picked up by new Kissing bug). Many reservoirs.

1)Chagas Disease-Inflamntn, swelling, facial rash/edema, death bea CNS damage (esp in chldrn) and myocarditis

Trypanosoma grucie g, rhodosaiense

Phylum ↓↓Nematodes↓↓

1)Found in 2/3 of world esp (sub)tropics and areas w/ ↓ sanitation 2)Most prevalent in Asia SthEast USA 3)4-14yos 4)Access to hlthcr, hygeine, soc.ec cond's also factors

1)Adult worms no acute ss(x) 2)GI obstr, abdom pain oral expulsion 3)Lung phase w/ pulmonary ss(x) (Ascaris coming out of anus?)

1)Temperate climates 2)5-10yos 3)Adults inhabit cecum Most common helminthe inf in USA

1)Enterobiasis-usu ass(x) but ss(x) = perianal pruritus at night, anorexia irritability abdom pain Sometimes fem w/ vulvovaginitis or peritoneal granulomas

1)Indigenous to S.E. USA (KY, TN, FL LA etc) esp veterans

1)Skin-Larva currens (fast advancing skin lesion usu on perineum or trunk 2)GI-bloating, anorexia nausea 3)Pulmonary-nonspcfc

1)inhabit lymph syst and subq tiss Larva is inf agent Tropical

1)ass(x) 2)Acute Lymphadenitis w/ fever Elefantitis(?)

Schistosoma mansoni hepslpleenomegally

Fasciolopsis buski Asia Metacercariae is inf agent

↓↓Class Cestodes↓↓General Features Head w/ scolex suckers, hermaphroditic, no gut, nutrients via abosrption aka Tapeworms


Taenia solium

Taenia saginata

Rickettsia and EhrlichiaI) Rickettiosis


Rickettsia prowazekii

R. typhi

Rickettsia rickettsii

wrldwde Humans only definitve host T saginata no hooks Larval cyst in undercooked meat is inf agent High in Latin America/Africa low in USA

1)T solium-passing of gravid proglottids >13branches/glottid thus major concern is develping cystercosis 2)cystercosis-depends on where cyst is Neuro is fatal

wrdwde High in Latin america low in USA T solium has hooks, Eggs of undercooked beef are inf agents

1)T sagomata-abd pain, passing proglottids 15-20branches/glottid 2)cystercosis-depends on where cyst is, Neurocyst can be fatal

Echinococcus granulosus

WrdWde Egg causes inf Larva causes dss Protoscolios inf dogs dogs poop eggs other wldlif/humans infected

Cystic echinococcosis Hydatid Cysts Can Be Found In Liver

Human/Rat Louse (or flea) (respectively) is vector/reservoir, Louse dies b/c of inf, Africa, S. America. No person-person transmission G(-)

A)Typhus Fever 1)Epidemic/Louse bornTyphus-Fever HA myalgia, rash on 4th day (1st on trunk then limbs usu not face), Maculopapular rash w/ petechia, CNS dsf(x)(stupor delerium), uremia Brill's Disease is remanifestation usu mild w/o rash

Texas G(-)

2)Endemic Flea Born Typhus-Same as Epidemic but less severe Rash first on appendages THEN trunk

E. USA, campers/hikers. Roden/Dog ticks are vectors. Ticks are vecrtor and reservoir. Ticks not killed by inf G(-)

B)Spotted Fever 1)Rocky Mt. Spotted Fever-incubation x 5days, HA fever myalgia, maculopapular rash w/ petechia on 4th day on hands feet then trunk face. Death via circulatory collapse/kidney failure

R. conoria G(-)

R. akari

Orienta tsutsugamushi

Cocellia burnetti

Ehrlichia ewingii Wisconsin, Minnesota E)HumanGranulocyticEhrlichiosis


2)Boutennese Fever milder form of RMSF Rash first on trunk then appendages

Transmitted by mite bite of house mouse G(-)

3)Rickettsialpox Rash first on trunk then appendages

SE Asia, Australia. Transmitted by chigger G(-)

C)Scrub Typhi Rash first on trunk then appendages

Farm/Rural area, Slaughterhouse workers

D)Q Fever Rash first on trunk then appendages

Actinomycetes

No Immune RE: b/c it's too far away. Reason for removal is usu. Cosmetic

Key Diagnostics Treatment Notes

Spirochetes

Spiral shaped, Nonsporulating, Motile


1)examin sputum, pus tissue, cervical exudates for granules and filaments >1mcmtr side. 2) Culture ID via morph, gram stain (+) and fimaments. 3)Facultative anaerobes

1)PNC 2)tetracycline, clindamycin, sulfonamides. 3)surgery to drain lesions

Part of normal flora. Propylactics used by

dentists and after trauma.Nonsporeforming

1)Distinguish from TB 2)Exam sputum for G+ orgs 3)Culture ID via morph, Aerobic growth, partial acid fast

1)SFM-TMP 2)surgery

20-30% fatal 1)Log phase more virulent vs stationary phase. Virulence due to penetrating growing tip.

Effect lysozome fx. Virulent forms grow out of

macrophage

1)Examine pus for granule and verify size, color, G+ w/ bact filaments<fungal filmts 2)Culture ID via morph, cell wall composition, use for verification

1)Long term antibx. PNC(Actinomyces), Chloramphenicol Sulfonamides (Nocardia) Streptomycin (Actinomadura, Streptomyces) 2)Amputation-last resort

inf by traumatic implantation

1)Direct exam 2)Serologic tests-NonspecificTrepanomal Rapid Plasma Reagin for cardiolipin, ELISA, Specific Trepanomal (hemaggltzn assay, fluoroscein antibody tests 3)Demonstration of orgsm via drkfld exam, silver stain, tests under "2)"

1)PNC, 2)Ttracycln, Erythromycin, 3)Jarishc Herxheimer Rxn

NonVenereal ss(x)-Yaws, Pinta, Bejel Dg(x) via demonstration of orgsm T(x)=PNC (or Ttrcycl or Erythrmc) 2)Virulence-Outer membr prots for adherence, hyaluronidase for tissue invasion, fibronectin for mimic, antiphagocytosis (reason for undetectable) 3)May cause still born or late abortion

Skin to skin

Skin to skin

Oral Microbiology


…?

Transmission via mouth-mouth contact Usu not fatal

Borrelia in blood, stain w/ Giemsa. Must take sample DURING febrile stage.

1)Ttrcycln, Erythromycin 2)JH rxn

Tick born is Endemic. Louse Born is Epidemic. Relapses progressively

milder. Death via CV probs

1)Clinical exam-"Bullseye erythema"(75% of p(t)) 2)Serological tests ELISA, Immunoflrsc Ab

1)Early Inf-Doxycycline or Amoxycilin 2)Late-Ceftriaxone

Can lead to debilitating arthritis

1)Darkfield microsc1)Long course antibx 2)Vaccinate livestock

Only spirochete resistant to envrnmnt outside body thus is the only spirochete that can be cultivated. Transmission via soil, H2O, food, inf tissue, congenital(rare)

Bact of supragingiva is mostly G(+) sp. Bact of subgingiva is mostly G(-) sp. Disruption of these proportions → disease.

1)Caries excavation. Restore missing s(x)

Legionella and Bartonella1)Peru Ecuador, Colombia 2)G(-) rods fastidious (needs humidity w/ CO2) 3)Spread via sandfly Phlebotomus


Gentamycin

Gentamycin

None

1)Flurosc antibody staining 2)Culture fr lung

1)Erythromycin 2) Rifampin

G(-) rods Stain better w/ silver stain Antiphagocytic Antibodies≠killing Cytotoxin inhibits PMN respiratory bursts Macrophages may kill Orgs produce B-lactamase Two other Legionella spp w/ diff DNA but same ss(x)

1)Can be found w/o dss.

1)Can be found w/o dss 2)may cause SBE

1)Blood ID esp in immcmpr pts 2)Cultures NOT helpful b/c too few orgs available due to cell mdtd RE

1)Now reduced in AIDS pts b/c of t(x) for M tb inf

Parasites


Phylum Ciliaphora

Phylum Apicomplexa

SubKingdom Protozoa↓↓↓

20μm. 1)Flask shaped ulcers in intestine 2)stool samples mcrscpy (watery-trophozoites w/ ingst RBC solid-cysts)--not helpful after dissemination 3)Ab testing, ELISA, PCR

1)Metronidazole (flagyl) follwd by iodoquinol 2)t(x) for carriers w/ luminal amoebiasis iodoquinol, furamide and paromomycin 3)Improve sanitation

Phylum Sarcomastigaphora Class Sarcodina NOT

commensal, Amoebic cysts can form in liver maybe

fatal, Reportable dss in Tx Asexual reprodx. Cyst

Ingestion→Stomach→HCl to release trophozoites in dudnem→Attachment to host cell and destruction

1)Exmn stool x trophozits (fresh smple) usu billions of trophzits, Smple at diff time intervals b/c neg sample ≠inf, Cysts are 11μm long commonly found in solid samples and survive for ≈2wks 2)String test, Ab test w/ 98% accuracy

1)Metronidazole, furazolidine, quinacrine. T(x) of contacts

Phylum Sarcomastigaphora Class Mastigaphora

Cyst*chlorine resistant* Ingestion→Stomach→HCl to release trophozoites in

dudnem and jjnm→trophzits attach to

intstn villi via ventral suckers and absorb

semidigstd food through body, usu encyst in colon, onset of dss b/c of intstn

inflmmtn.

1)Exmn RBC's for rings 2)PCR or Ag detction

1)Mefloquin-orally Quinine-IV both to treat blood and liver

↓↓↓SubKingdom Metazoa↓↓↓


Phylum Platyhelminthes Class ↓↓Trematodes↓↓ Nutrient uptake via absorption Nonsegmented


1)Ab testing, IgM (not found in AIDS p(x))

1)"Nml" pt-Clindamycin 2)AIDS pt-Pyrimethamine w/ Trisulfapyrimadine 3)Pregnant-Spiramycin

Prevention via good hygiene and women

avoiding cat litter

1)Thk/Thn blood films for trypomastigotes 2)Biopsy-of nodes, spleen, liver for amastigotes 3)xenodiagnosis-inf clean kissing bug w/ p(t) blood

1)Nifurtimox (has little affect on tissue inf) 2)Na Stibogluconate w/ Meglumine antimoniate

Kissing bug eradication as control method

Phylum ↓↓Nematodes↓↓

1)Microsc ID of eggs in stool 2)Poor growth

1)Albendazole PO (mebendazole later to treat whipworm), Mebendazole avoid vermifuges 2)VitA to improve growth devl't

1)Fem > Male 2)15-35cm long Creamy white Cuticle w/ fine circular striations 3)Adult lives in upper sm

intest

1)Nocturnal observation 2)Scotch tape test of anal area and view micrscp for eggs (≈50mcrmetrs)

1)Albendazole PO (mebendazole later to treat whipworm), Mebendazole 2)treat whole family and school chums

1)F>M 2-13cm Yellow, Fem w/ pointed tail 2)Gravid fem migrates to anus to deposit

eggs 3)Hygeine preventative

1)Eosinophilia as hallmark of helminthe inf 2)Larva in stool 250μm orgnsm=intestinal inf 600μm orgnsm=hyperinf 3)Larva in sputum = hyperinf 4)Culture in beef broth

1)Ivermectin or Thiabendazole, but usu too late by the time p(t) seeks t(x)

1)Symptoms can occur if p(t) put on corticostrds 2)worms don't need to leave body to finish life cycle Can also be free

living 3)↑ prodx of steroids → ↑ virulence

1)Microsc ID of mcrofiliariae of blood sampls at night 2)ICT for Ab-Ag rxn.

1)interruption of dss w Albendazole+Ivermectin(or Diethylcarmazine) for 5 yrs Alleviate/prevent-lymphedema mngnmt

blood/tisse parasite Mosqo vector

↓↓Class Cestodes↓↓Head w/ scolex suckers, hermaphroditic, no gut, nutrients via abosrption aka Tapeworms


Rickettsia and EhrlichiaI) Rickettiosis


eggs w/ spine in feces

Praziquantel (incr cell membr permeability) Oxamniquine no longer available in USA

vaccine dev'lt against Sm p80 would be nice avoids inf via surf membr renewal

elliptoid shaped eggs in stool or vomit

Praziquantel (incr cell membr permeability)

1)worm inf dgx via eggs in stool 3mos post inf ID of progolittid for speciation 2)cystercosis-cysts in involved organ Eggs in feces Ag-Ab tests

1)Praziquantel for worm inf. 2)Albendazole or Praziquantel for cystercosis 3)Surgy to remove calcified cysts

cysticercosis ingestion can happen in populations that don't eat pork. b/c a carrier can contaminate the nonpork meal e.g. jews eating food from a dirty pork eater

1)worm inf dgx via eggs in stool 3mos post inf ID of progolittid for speciation 2)cystercosis-cysts in involved organ Eggs in feces Ag-Ab tests

1)Praziquantel for worm inf. 2)Albendazole or Praziquantel for cystercosis 3)Surgy to remove calcified cysts

Imaging Serological tests should be used b/f invasive methds, Immunoassys

Surgry w/ postop Albendazole

Flea born Typhus-Rash on arms/legs THEN trunk Tick born-Rash on trunk first then legs/arms, serology

Ttcycl, Chloramphenicol w/in 7 days onset

30%fatal Flea born Typhus is wrdwde Not fatal for fleas. Fatal for louse



inf in tick is everywhere, <60%fatal w/o t(x). Rickettsia live in nucl of cell 2 and 3 caused by diff sp vs 1)







Severity of dss b/c of high [endotoxin] Vector control important esp for human lice and rats Vaccine available

Superficial InfectionsGeneral Features No Immune RE: b/c it's too far away. Reason for removal is usu. Cosmetic


Trichosporon beigelii

Exophiala werneckii

Malassezia furfur

Cutaneous Infections (Dermatophytosis)

General Features


M. audouinii

T. tonsurans

common in Mediterranean

M. audouinii children, worldwide

usu males. Favors humidity

Trichophyton

usu occurs w/ tinea pedis

More Notes:

Subcutaneous InfectionsGeneral features Introduced via traumatic implantation. Some occur worldwide w/ endemic areas, Several sp may cause same ss(x)Etiology Epidemiology Manifestations

Pedraia hortai Black Piedra-Black gritty nodules in hair shaft

Temperate climates, sporadically in S. U.S.

White Piedra-soft, mucilaginous, light colored nodules on hair

Teenagers, female, U.S. Gulf Coast, FL, warmth of Caribbean

Tinea nigra-Chronic asymptomatic infection of stratum corneum usu of palm

Normal skin/scalp flora. Ds(x) hightest in tropics. Found equally in wo(men). Recurrent. Excess perspiration, corticosteroids, malnutrition and hydrophobic cmpds on skin.

Pityriasis versicolor-Chronic, mildly asymptomatic non-inflammatory infection of stratum corneum. Lesions covered w/ sharply delineated furfuraceous scales, w/ variable pigmentation, may be single or coalesed.

usu caused by 1) Trichophyton (rubrum, tonsurans, mentagrophytes) 2) Epidermophyton floccosum or 3) Microsporum (canis, gypseum, audouinii). colonize keratized tissue. Found on humans, animals, and in soil. Inf fr nml flora are more chronic/mild. Inf fr soil/animals more acute, more sensitive to t(x) and less likely to reoccur. same sp can cause more than one ss(x), more than one sp can cause same ss(x).

childhood disease. Spread frm Mexico to U.S.

Tinea capitus-1) Epidemic a. Grey patch caused by M. audouinii b. Black dot caused by T. tonsurans 2) Nonepidemic more severeTinea favosa-yellow cup shaped crusts called scutula

occurs in adult males, acquired from animals

Tinea barbae-mild irritation to folliculitis

Tinea corpus-ringworm on body w/ scaling to inflammatory lesions of glabrous skin

Tinea crurus (jock itch)-Lesions are sharply demarcated raised erythematous border

Most common, affects millions worldwide

Tinea pedis (athletes foot)-…often begins on 4th/5th digit

Tinea manum-infection of hand

Tinea unguium-nail infection

Transmission my contact, either fr soil, lesions, or indirect (pool, shower, comb, etc) Microsporum sp:macroconidia, Epidermophyton floccosum:macroconidia, Trichophyton sp:microconidia. Temp sensitive limits inf to surface. Fatty acids on scalp after puberty help limit grey patch to pre-puberty.

Sporothrix schenckii

Rhinosporidium seeberi

Loboa loboi

Entomophthoromycosis (C/B?)

Systemic Infections

General Features


Found worldwide, endemic areas in Brazil, Mxco, Zimbabwe. 75% of cases male, in U.S. associated w/ horticulture/gardening as occupational hazard.

Sporotrichosis-4 clinical types: 1) cutaneous lymphatic-75% of cases. Leads to necrotic lymph nodules progressing along lymph vessels 2) cutaneous non-lymphatic-"fixed" form, found in endemic areas

Pseudallescheria boydii

1ly in males b/c of exposure. Wolrdwide w/ endemic areas in Sudan, Mxco. Orgms usu live in soil.

Mycetoma (Eumycetoma)-localized, swollen, lesion with pus on foot or hand. Pus contains grains. Looks like random lesions on body with dark, crusty draining blotches.

Fonsecaea pedrosoi, Phialophora verrucosa, Cladosporium carrionii

Worldwide, more in Tropics. Males>Femes. Usu a soil orgnsm. Inf via traumatic implantation

Chromo(blasto)mycosis-SubQ, localized chronic inf of skin and subq tissues leading to verrucoid, ulcerated, crusted l(x)s. Starts as small red macule then black stuff on skin, then HUGE swollen warts.

Cladosporium trichoides, Fonsecaea pedrosio, Bipolaris spicifera

Phaeohyphomycosis cerebral-1)SubQ Phaeo is subQ cysts (1"x1") red, black 2)Cerebral Phae is cerebral inf w/ abscess, fatal 3)inf of paranasal sinuses

Aquatic parasite. Occurs in children/young men > femes. Most cases in Sri Lankan divers/fisherman

Rhinosporidosis-looks like huge wart on/near nose

Affects males, usu S. America. Dolphins may be resorvouir

Lobomycosis-chronic inf may spread peripherally w/ verrucous ulcerated lesions. Develops over 20-30 yrs

Conidiobolus coronatus or Basidiolus ranarum

1)Occur in nml hlthy peeps, asymptomatic/subclinical 2)1ly pulmonary inf that may spread via blood 3)immunit to reinf 4)geographically restricted or in endemic areas 6)localized outbrx from exposure to common source

Coccidioides immitus, Coccidioides posadasii

white females, immunocompromised (AIDS). Disseminated form occurs in men w/ pigmentation and pregn femms (3rd trimester). Found in Sonoran Life Zone/Desert (e.g. El Paso) SW U.S., Mexico. C immitus in San Joaquin Valley. C posadassi elsewhere. Thermly dimorphic mold-soil.

Coccidiomycosis-1)1ry inf is generally inapparent, benign (60%) or mild-severe URI. 2)2ry inf (a)benign chronic pulmonary-thin walled cavities or granulomas (b)progressive pulmonary form-may follow 1ry or from reactivation. May disseminate to skin depending on health status

Histoplasmosis capsulatum

Incidence: Symptomatic pulmonary disease 75% Men. 1:1 sex ration in chldrn. Mildly chronic cases are 75-90%male. Immunocompromised p(x) at risk or mortatlity 70% dissemination and mortality in AIDS p(x). Sexual bias in disease but not exposure Geography: Worldwide, endemic areas E of Misspi, incldng Rio Grande areas. Mold-soil microconidia-irrittion on inhalation. Animals as reservoir.

Histoplasmosis-1)pulmonary inf 95%subclinical. Leaves cavitary lesions in peeps w/ underlying lung probs 2)Disseminated disease may leave lesions b/c infd retic.edoth cells freely disseminate even in ass(x) p(x). Oropharyngeal cancer due to mildly chronic disase (recurrent over 10-20yrs). 3)African Histoplasmosis disese of skin and bones

Blastomyces dermatitidis

Incidence: males>femms AfroAmrcns> All ages but more in 30-50yo's In small epidemics-no sex bias, mostly children inf, usu pulmonary inf. Geography: Thermally dimorphic, Africa, Mxco, Venzla, Israel, India, East U.S. Coast. Lives in soil. Animals (dogs) as reservoir.

Blastomycosis-Inhalation of conidia → 1)Pulmonary inf w/ variety of ss(x). 2)Chronic cutaneous disease is 80% of presentation w/ 50% having pulmonary ss(x) 3)Disseminated disease generalized w/ bone, UG tract, and CNS as extrapulmonary sites.

Paracoccidioides brasiliensis

Incidence:No sexual bias w/ 5-25% of pop skin test +. Symptomatic disease are 90%male ag wrkrs. 11:1 male:femm b/c estrogen inhibits mold to yeast morph. Geography:Central and S. Amrca. Avoids the Amazon Thermally Dimorphic

Paracoccidiomycoses 1)Pulmonary inf asymptomatic, self limiting, may become latent, few develop ss(x) after exposure. 2)Chronic Progressive Inf occurs following latency in 90% cases w/ dissemination to mucosal and gingival srfcs, may have chronic pulmonary disease and some both Dissemination to other organs also observed 3)Acute progressive form (10%of cases) in children and adults fatal in weeks

Opportunistic InfectionsGeneral Features 1)Inf of immunocompromised 2)becoming more frequent 3)pathogenic ones are ubiquitous 4)any fungus or shroom may cause inf


Cryptococcus neoformans va grubii

Incidence:most children in NY cty skin test +, 1000cases/yr in nonAIDS pop. Maybe 3:1 male:femms. 50%in healthy peeps, 50% 2ry to DM, AIDS, bone cancer, 4th most common disease in AIDS p(x) Geography:worldwide types B-tropical, type C-S. Calif, type AandD-soil and pigeon guano (pigeon as reservoir) Yeast is inhaled and forms capsule after infection

Cryptococcosis-1)1ry Pulmonary inf usu ass(x) to mild ss(x) thus not often diagnosed 2)Disseminated disease-meningitis in U.S., skin/bone inf-Euro.

Candida albicans, and other sp

1)Nml flora of mouth, GI, vagina, skin 2)immunocompromised, trauma experience e.g. burn, leukemias, endocrine factors e.g. DM/DI, AIDS are all predisposing factors. Also iatrogenic 3)Plaque made of (an)aerobe leading to microenvironment. Deep seated plaque required physical scraping for removal. Biofilm helps colony grow. Abiotic surfaces e.g. dentures, help biofilm adhesion and device deterioration

Candidasis-Thrush, Vaginitis, Intertrigginous, Onychomycosis, Diaper rash 2)Systemic inf 4th most common nosocomial blood stream inf and is life threatening. 3)Endocarditis 4)Recurrent Eye inf 5)Random skin rashes/lesions after sepsis 7)UTI 8)chronic mucocutaneous candidiasis involved cell mediated immunity. epithelial lesions are verrucous and warty

Aspergillus fumigatus and other sp.

Adults, males-unkown sex bias 2)similar predisposing factors as Candida. 3)Worldwide in soil-mold, decaying vegetation, can be aerosolized

Aspergillosis-1)Allergic RE (IgE) as asthma, allergic bronchopulmonary aspergillosis (most common RE), IgG RE for nonatopic inf 2)noninvasive colinization-aspergilloma in preexisting cavity e.g. pulmonary pleura, asymptomatic may lead to fatal hemmorrage, nonpulmonary colonization in head cavities w ss(x) of otitis, sinusitis etc. 3)Invasive disease occurs as 1ry pulmonary inf of compromised host seen as a fatal necrotizing pneumonia, dissemination may spread to GI, liver kidney etc

Pneumocystitis jiroveci

More Notes

Rhizopus orysae, Absidia, Rhizomucor, Mucor

Predisposing factors: Acidosis-rhinocerbral inf, Leukemia Steroids Immunosupprsant-thoracic form Geography:Worldwide on decaying vegetation-mold, soil, H2O. Produce sporangiospores (conidia)

Muromycosis-1)Cerebral form looks like bells palsy, death w/in 1 week if untreated 2)Thoracic form is usu pulmonary inf.

Immunocompr, AIDS p(x), Ubiquitous, Worldwide, nml flora, animals as reservoir 30-40%mortality in infants, 10% mortality in AIDS p(x)

Pneumocystitis jiroveci Pneumonia-Diffuse pneumonia 1)debilitates infants w/ subtle infant, Bcell and Lymphocyte infiltration 2)immnocopmr p(x) manifest ofver several weeks w/ fever, recurrent/breakthrough tachypnea, massive # of orgnsms invading alveolar spaces.

Nosocomial inf x2 fr 1980-1990 at 4/1000 discharge. Candida albicans 60%, Candida sp. 20%, Torulopsis, Aspergillus.Inf of UTI, surgical wound, pneumonia, fungemia, IV catheter most likely cause for inf. Infectious, and expensive. Other opportunistic sp: Trichosporon (see white piedra), Geotrichum, Penicillium

Superficial InfectionsNo Immune RE: b/c it's too far away. Reason for removal is usu. Cosmetic


Hair cut (or Terbinifine)

Cutaneous Infections (Dermatophytosis)


Subcutaneous InfectionsIntroduced via traumatic implantation. Some occur worldwide w/ endemic areas, Several sp may cause same ss(x)


Direct exam shows hair shaft w/ nodules. Under scope shows fungi

These are types of Piedra

1)Examine skin scrapings for pigmented hyphae. 2)Culture for verification

Topicals: miconazole, ointment, sulfur soln's, salicylic acid

Can be confused with malignant melanoma

examine skin scales for shory hyphae and spherical cells

Topicals: 1)SeSulfide micon/ketocon(azole) Oral: ketocon/itracon/flucon(azole)

lipophilic, hypopigmentation due to interference of fungal melanin synths

mentagrophytes) 2) Epidermophyton floccosum or 3) Microsporum (canis, gypseum, ). colonize keratized tissue. Found on humans, animals, and in soil. Inf fr nml flora are more chronic/mild. Inf fr soil/animals more

acute, more sensitive to t(x) and less likely to reoccur. same sp can cause more than one ss(x), more than one sp can cause same ss(x).

USEFUL FOR MOST: 1)chronicity 2)reoccurence 3)severity 4)spread to others 5)pets/animals 6)distinguish fr C.albicans. Some sp fluoresce so use "wood's lamp". Examine hair for spores (endo/ecto(thrix). Skin/nail scraping for hyphae. Culture ID via color, txtr, topography etc)

1)Topical nonRX-Undecylenic acid, Tolnatrate, Miconazole, Clotrimazole, Terbinafine, Drying cmps, keratolytic agents. nonRx often used b/f seeing a physician. 2)Topical Rx-Exonazole nitrate, Ketoconazole, Oxiconazole, Sulconazole, Ciclopiroxolamine (nail lacquer) Naftifine, Butenafine 3)Systemic-Griseofulvin, Detoconazole, Itraconazole.

usu aquired fr animals (dogs)

less common nowadays

may require antibacterials for 2ndry inf

Transmission my contact, either fr soil, lesions, or indirect (pool, shower, comb, etc) Microsporum sp:macroconidia, Epidermophyton :microconidia. Temp sensitive limits inf to surface. Fatty acids on scalp after puberty help limit grey

Surgery

Systemic Infections


Lesions along lymphatics is pathognomonic. Direct exam for cigar shaped yeast. Culture ID of thermally dimorphic (grows as: mold in soil, yeast at 37º. Serology not helpful

Orally-KI (in milk), Itraconazole Topical-Amphotericin B (for lymphatic relapse or 1ry pulmonary inf, Heat

1) looks like cysts on skin following lymphatics 2) looks like you put your skin through a meat grinder. Dissemination is rare. Pulmonary inf is becoming common in hospitals

Direct exam of pus for granule of certain size, color, filaments >1mcromter. Culture for verification based on morphology and asexual conidial formation

1)Longterm antib(x): Ampho B, topical Nystatin, KI (all w/ little success). 2)Surgery to clean abscess. 3)Amputation.

Actinomycetoma is due to bact. yeast grows faster vs mold

Direct exam reveals pigmented branching hyphae w/ sclerotic bodies (spore). Culture ID of dark pigmented colonies looking for asexual reproduction

1)Surgery successful if early 2)Itraconazole 3)Antibacterials for 2ry inf 4)AmphoB-partial cure w/ relapse

Direct exam of tissue shows pigmented fungal elements Culture ID via morphology and conidial formation

Drugs w/ variable success. Surgery for certain manifestations

Cerebral Phaeo diagnosed after death.

6-330 mcrmtr sporangium (filled w/ endospores) No culture available

1) Surgery 2) various drugs tried

Direct exam of tissue for chain of bout 4 lemon shaped cells bout 9micrmeters. No culture

Similar to chromomycosis

Spontaneous resolution

1ly pulmonary inf that may spread via blood 3)immunit to reinf 4)geographically localized outbrx from exposure to common source

Skin test. Differentiate from other URI's. Take travel h(x). Direct exam of sputum for sporangia or spherules. Thermly dimorphic grows as spherule-tiss. Culture ID for arthrospores in filament (also exoantigen and DNA probe)

1)bed rest for 1ry ss(x) 2)disseminated w/ AmphoB or Fluconazole (use Fluc in AIDS p(x)) 3)cavities removed surgcly

HIGHLY INFECTIOUS. Possible terrorist agent. Virulence due to protease, estrogen binding prot, Tcell mediated RE in reinf, alkalinazation of phagosomeallergies to 1ry inf is good b/c it indicates immune RE.

1)Direct exam of sputum, biopsy, blood for intracellular yeast. Culture ID takes 28 days shows spores w/ spikes. Use DNA probe nstead 2)animal inoculation to obtain tissue for ID. Blood test also helpful for d(x) and pr(x)

1ry Pulmonary-treat ss(x) only. Acute cases use AmphoB or Itraconazole w/ Ketoconazole and fluconazole as alternatives. Surgery to remove pulm lesions

moderate chronic disseminated disease fatal if untreated (6-12 mos) Fulminant disease may occur in infants and adults. Resistant to oxidative burst

1)Direct exam of sputum, biopsy, pus, for broad based budding yeast 2)Culture ID yeast-tissue mold-nature 3)DNA test, exoantigen

1)AmphoB Itrazonazole 2)2hydorxystilbamine 3)Ketoconazole-mixed results 4)Itraconazole for HIV suppression

virulenc factors: morphogenesis, cell wall, anti macrophage adhesion

1)Direct exam of mucosal scrapings for "pilots wheel" yeast 2)Culture ID mold-nature yeast-tissue, ID via yeast form 3)serolgy for diagnosis/prognosis

1)Sulfa drugs x 3-5yrs 2)Imidazoles, oral kitoconazole (possiblity of relapse) Itraconazole 3)AmphoB for inpatient

Skin test shows no sex bias for symptomatic disease Virulence factors:morphogenesis, estrgn binding prot, cell wall, immune suppression

Opportunistic Infections1)Inf of immunocompromised 2)becoming more frequent 3)pathogenic ones are ubiquitous 4)any fungus or shroom may cause inf


1)Direct exam of sputum or CSF in India ink for capsule 2)Culture ID-cells examined for capsule Phenol oxidase test used for ID 3)Serologic test for capsular antigen.

1)AmphoB 2)Combo AmphoB+5-Fluorocytosine 3)Fluconazole (esp in AIDS p(x) to prevent relapse)

1)only fungus w/ capsule 2)Meningitis fatal if untreated 3)Virulence factors:Mating type, growth at 37 degr, capsule is antiphagocytic, immune suppression

1)Direct exam of sputum, pus, tissue for yeasts, pseudohyphae 2)Culture ID looks for germ tubes, chlamydospores. Yeast ID via physio rxns 3)Isolation from skin/vaginal mucosa to confirm. Significance in urine 'pends on other factors Isolation fr sterile site significant. 4)Serology ineffective

1)Topicals for Cutaneous-Nystatin, Miconazole, Clotrimazole(OTC x vaginitis), Ketoconazlole. 2)Thrush t(x) lozenges 3)Esophegitis AmphoB, Fluconazole 4)Systemic-AmphoB, Fluconazole, Ketoconazole (sometimes combo w/ Miconazole IV and 5-Flurocytosine 5)t(x) of predisposing factors helps in t(x)

1)can be acute/chronic, disseminated/superficial/deepseated 2)Concern of esophigitis in AIDS 3)Virulenc Factors:yeast morph chgs, protease phospholipase, adhesins, laminin collagen, macrophage evasion, immune supression, Th1 response and Th2 susceptibility

1)Direct exam of sputum, biopsy for septate hyphaew/ acute angle branching 2)Culture ID based on colonial morphology and pattern. Fast growth (white center, green cortex) +blood culture should be considered significant since even invasive cultures can be - Serologic test best in noninvasive disease

1)Treat allergy ss(x) 2)AmphoB w/ 5Fluorocytosine or surgery for Aspergilloma 3)Must treat invasive disease aggressively b/c it's fatal. AmphoB or Itraconazole

1)ubiquitous so may be contaminate in culture so repeated cultures used. 2)Virulence:protease phospholipase, adhesins laminin, gliotoxin (immunosuppresant) endotoxin

1)Direct exam of sputum, biopsy for NON-septate hyphae, usu few to see 2)Culture ID via colony morphgy and sporangial formation

Disease fatal w/o t(x). 50% w/ t(x) 1)AmphoB 2)surgical debridement

1)Direct exam-Infant looks emaciated, X-rays show diffuse lung cavity 2)sputum, Biobsy (for asci, spores ameboid shaped yeast, 3)No culture available

1)Acute t(x) Trimethoprim-sulfamethozoasole 2)Propylaxis for AIDS via TMP-SMX.

Fungus related to ascomycetes. Atypical chrtcs, used to be thought as parasite. Virulence:adhesins to Type I pneumocytes, disruption of blood-air barrier (lung)

Candida albicans 60%, Candida sp. 20%, Torulopsis, Aspergillus.Inf of UTI, surgical wound, pneumonia, fungemia, IV catheter most likely cause for inf. Infectious, and expensive. Other opportunistic sp: Trichosporon (see white

Topicals* Orals+ IV^

Undecyclin Griseofulvin EchinocandinHaloprogin 5-flurocytosine Miconazole*^Clioquinol Nikkomycin Z Fluconazole*^Triacetin Ketoconazole*+ Voriconazole+^Ciclopiroxolamine Fluconazole*^ Amphotericin B*^

Itraconazole

Voriconazole+^

Squalene 2.3, epoxidase inhibitors (tolnaftate, naftifine, terbinafine, butenafine)

Allyl Ammines are

part of the Squalene

2,3 epixidase

inhibitors

(Terbinafine,

Naftitine,

Butenafine)

Polyenes* (Nystatin, Amphotericin B*^)

Azoles*+^ (Clotrimazole, Econazole, Ketoconazole *+, Miconazole *^, Butoconazole, Oxiconazole, Sulconazole, Terconazole, Tioconazole)

Drugs for Superficial Infections

Drugs for Cutaneous Infections

Drugs for SubCutaneous

Infection

cell wall synths cell wall f(x) DNA syns

Azoles

Naftifine Clotrimazole*Terbinafine Econazole*Butenafine Fluconazole*^

ItraconazoleKetoconazole*Miconazole*^

Oxiconazole*

Sulconazole*

Terbinifine*+

Terconazole*TioconazoleVoriconazole+^

Allylamines of the

Squalene 2,3

epoxidase inhibitors

Drugs for Systemic Infection

Drugs for Opportuinistic

Infection

DNA synssqualene epoxidase inhibitors

Polyenes

NystatinAmphotericin B*^

competition for subst

DNA Viruses

Enveloped Naked

Poxviridae Herpesviridae Hepadnaviridae Adenoviridae Papillomaviridae Polyomaviridae

Variola Vaccinia Monkeypox Molluska contagiosum HSV VZV EBV CMV HHV Hebatitis B Adenovirus HPV JC BK Simian Parvovirus B19 Adenoassociated virus

Parvoviridae *ssDNA

A11

hugolaptop: along w/ paramyxo, the largest viruses ≈ 300mcrmeters

P15

hugolaptop: smallest virus

RNA Viruses

ss RNA

(+) RNA (-) RNA

NonSegmented Nonsegmented Segmented

Naked Enveloped Enveloped Enveloped

Picorividae Noroviridae Togaviridae Flaviviridae Coronaviridae Retroviridae Parmyxoviridae Filoviridae Rhabdoviridae Arenaviridae Bunyaviridae Orthomyxoviridae

Rhinovirus Poliovirus Echovirus Hepatitis A Norwalk Calciviridae Rubella EEV WEV VEV Yellow Fever virus Dengue Virus St. Louis virus Corona SARS HIV, HTLV 1 and 2 Parinfluenza Measles Mumps RSV Ebola Marburg Rabies VSV LSV TCV LCV CLEV Hanta virus Influenza A, B, CCoxackie Virus A and B

West Nile virus

Table 8-4. Transmission and Distribution of Pathogenic Parasites

Organism Infective Form Mechanism of Spread

Intestinal ProtozoaEntamoeba histolytica Cyst/trophozoite Indirect (fecal-oral)

Direct (venereal)Giardia lamblia Cyst Fecal-oral routeDientamoeba fragilis Trophozoite Fecal-oral routeBalantidium coli Cyst Fecal-oral routeIsospora belli Oocyst Fecal-oral route

Oocyst Fecal-oral route

Enterocytozoon bieneusi Spore Fecal-oral routeUrogenital ProtozoaTrichomonas vaginalis Trophozoite Direct (venereal) routeBlood and Tissue Protozoa

Cyst/trophozoite Direct inoculation, inhalation

Sporozoite Anopheles mosquitoPyriform body Ixodes tick

Toxoplasma gondii Oocysts and tissue cysts Fecal-oral route, carnivorismPromastigote Phlebotomus sandfly

Trypanosoma cruzi Trypomastigote Reduviid bugTrypanosom brucei Trypomastigote Tsetse flyNematodesEnterobius vermicularis Egg Fecal-oral route

Ascaris lumbricoides Egg Fecal-oral routeEgg Fecal-oral route

Trichuris trichiura Egg Fecal-oral routeAncylostoma duodenale Filariform lava

Necator americanus Filariform larva

Strongyloides Filariform larva

Trichinella spiralis Encysted larva in tissue CarnivorismWuchereria bancrofti Third-stage larva MosquitoBrugia malayi Third-stage larva MosquitoLoa loa Filariform larva Chrysops fly

Third-stage larva Biting midges or black fliesOnchocerca volvulus Third-stage larva Simulium black flyDracunculus medinensis Third-stage larva Ingestion of infected cyclopsDirofilaria immitis Third-stage larva MosquitoTrematodesFasciolopsis buski Metacercaria

Fasciola hepatica Metacercaria Metacercaria on water plantsMetacercaria

Metacercaria

Cryptosporidium species

Naegleria and Acanthamoeba species

Plasmodium speciesBabesia species

Leishmania species

Toxocara species

Direct skin penetration from contaminated soil

Direct skin penetration, autoinfection

Direct skin penetration, autoinfection

Mansonella species

Ingestion of metacercaria encysted on aquatic plants

Opisthorchis (Clonorchis) sinensis

Metacercaria encysted in freshwater fish

Paragonimus westermani

Metacercaria encysted in freshwater crustaceans

Cercaria

CestodesTaenia solium

Taenia saginata Cysticercus Ingestion of cysticercus in meatDiphyllobothrium latum Sparganum Ingestion of sparganum in fish

Embryonated egg

Embryonated egg

Hymenolepsis nana Embryonated egg Ingestion of eggs; fecal-oral routeHymenolepsis diminuta Cysticercus

Dipylidium caninum Cysticercus Ingestion of infected fleas

Schistosoma species Direct penetration of skin by free-swimming cercaria

Cysticercus, embryonated egg or proglottid

Ingestion of infected pork; ingestion of egg (cysticercosis)

Echinococcus granulosus

Ingestion of eggs from infected canines

Echinococcus multilocularis

Ingestion of eggs from infected animals, fecal-oral route

Ingestion of infected beetle larvae in contaminated grain products

Table 8-4. Transmission and Distribution of Pathogenic Parasites

Distribution

Intestinal ProtozoaWorldwide

WorldwideWorldwideWorldwideWorldwideWorldwide

North America, EuropeUrogenital Protozoa

WorldwideBlood and Tissue Protozoa

Worldwide

Tropical and subtropical areasNorth America, EuropeWorldwideTropical and subtropical areasNorth, Central, and South AmericaAfrica

NematodesWorldwide

Areas of poor sanitationWorldwideWorldwideTropical and subtropical areas

Tropical and subtropical areas

Tropical and subtropical areas

WorldwideTropical and subtropical areasTropical and subtropical areasAfricaAfrica and Central and South AmericaAfrica and Central and South AmericaAfrica, AsiaJapan, Australia, United States

TrematodesChina, Southeast Asia, India

WorldwideChina, Japan, Korea, Vietnam

Asia, Africa, India, Latin America

Africa, Asia, India, Latin America

Cestodes

WorldwideWorldwide

WorldwideWorldwide

Worldwide

Pork-eating countries: Africa, Southeast Asia, China, Latin America

Sheep-raising countries: Europe, Asia, Africa, Australia, United States

Canada, Northern United States, Central Europe

Nephritic = Blood + HTN + Oliguria + Azotemia + Edema

PSGN - Follows group A β hemolytic strep infx, usu due to bad hygiene, ↓ C3, ASO or antiDNAse B positive, shows "lumpy bumpy" on subepithelium w IF, large hypercellular glom

RPGN - Crescents → deposition of fibrin in bowman space, monocytes, large pale kidneysType I - Anti GBM IgG complexes → complex deposits on GBM → smooth linear appearance on

immunofluroscence. e.g Goodpasteurs

Type II - Immune complex mediated → "lumpy bympy" glomerular BM on immunofluorescence. e.g. Bergers Disease

Type III - ANCA associated aka Pauci immune shows nothing on GBM w immunofluorescence but PMNs have either c-ANCA or p-ANCA. Usu a RE to Wegener Granulomatosis or vasculitis'.

Alport Disease - mutation of α 5 Type IV collagen → nephritis, nerve deafness, and ocular problems and splitting of lamina densa

Hypercellular

Perihilar

Collapsing

Tip Lesion

Lupus NephropathyType I - no ssx

Type II - IgGs and C3 in mesangial matrix, Proteinuria, hematuria. Just uncomfortable

Type V - Looks just like MG

Nephrotic = Proteinuria +Hypoalbuminemia + Edema + Hyperlipidemia + Lipiduria

MCD/MN/nil disease/Lipoid Nephrosis - Fused/absent podocytes (epithelial foot processes)

FSGS - glomerular sclerosis frm persistent glomerular vasodilation

Membranous Glomurlonephropathy/MN/Membranous Nephropathy/MGN - subepithelial immune complex disease vs GBM but NO Ig's in ciruculation, epimembranous spike and dome appearance, Autoimmune states or heavy metals can predispose

Membranoproliferative Glomerulonephritis/MPGN - basement membrane alterations, glomerular cell proliferation, WBC infiltration,Tram Track appearance due to GBM duplication

Type I - Subendothelial IgG and complements, Prominent Tram Track appearance, ↑ mesangial cells, ganular complement deposits w IF, Ig complexes circulating

Type II - Dense Deposit Disease shows some tram trac appearance, C3 next to dense deposists, ↓ serum C3, no Ig's in BM complexes, IgG vs C3 convertase, ribbon like deposits w/in capillary,

nephrotic and nephritic ssx both present

Diabetic Nephropathy - Early stage has large kidneys (later has small granular kidneys), EM shows thick holey GBM, thin lamina rara interna and externa, tubular atrophy

Type III - Focal Proliferative has extenseive damage, ↓ complement, few pts w nephrotic ssx, segmental necrosis, mesangial deposits

Type IV - Diffuse Proliferative is most severe form, combo of nephritic and nephrotic ssx, 100% glomeruli involved, scarring, wire loop abnormalities, subendothelial depostis of Ig's and C3 and

Fibrin

HIV Associated Nephropathy - Black Drug users affected, Tamm Horsfall prots

IgA Nephropathy/Berger Disease - IgA deposits in medangium, recurrent hematuria

Amyloidosis - large kidneys, low BP, congo red stain positive

Hypertensive Nephrosclerosis - Black ppl w uncontrolled HTN, proteinuria

AnticonvulsantsDrugs That Work On Na+ Channels

Drug MOA SDFX Source T(x) For

Carbamazepine

Oxcarbazepine Same as CBZ but less frequency notes

Lamotrigine Inactivates Voltage gated Na+ channels notes

Drugs That Work On T-type Ca++ ChannelsDrug MOA SDFX Source T(x) For

Zonisamide notes

Hepatic Toxicity

Phenytoin (Fosphenytoin is broken down into Phenytoin)

Decrease Influx. Increase Efflux of Na+, Ca2+ and K+ channels in open state

Nystagmus, Diplopia, Ataxia, Hirsuitism, Coarsening of Facial Features, Mild Peripheral Neuropathy

Website

Anticonvulsant (Partial and General Tonic/Clonic Szr)

Slows recovery rate of inactive Na+ Channels, preventing the PDS. Metabolite also active. paroxysmal depolarizing shift

Dizzines, diplopia, nausea, ataxia, blurred vision. Aplatstic anemia, Agranulocytosis, Thrombocytopenia, StvJohnson Sx

Website

DOC: Anticonvulsant (Partial Szr), Anticholinergic, antineuralgic, antidiuretic, muscle relaxant and antiarrhythmic

Metabolized to active cmpd 10, 11Dihydro-10 Hydroxy-5H Dibenz[b,f]azepine5Carboxamide

Same as CBZ Partial Szr

Dizziness, HA, Diplopia, Nausea, Somnolence, Skin Rash (may progress to StvnJohnson Sx). Increased risk of cleft palate if used during pregn.

Monotherapy in Partial Seizures (also in adjunct to Valproate acid); Absence & Myoclonic szrs in children

Blocks Na+ channels & decreases Cl- flux via T-type Ca++ channels

StvnJohns Sx, Contraindicated in ppl w/ allergies to sulfonamid AB

Adjunct thpy for Partial Szrs as induction NOT long term use

Valproic Acid (GABA synth inducer)

At low conc. Blocks voltage Na+ channels. High conc slows influx of Ca++. Increases activity of GABA making enzm (glutamic acid decarbxlylse) and inhibits GABA metabolism.

DOC: Generalized Epilepsy Sx. Absence Szr

http://metagenics.com/resources/imc/OneMedicineProf/ProfDrugs/Phenytoinpd.html#mechanism-action

http://metagenics.com/resources/imc/OneMedicineProf/ProfDrugs/Carbamazepinepd.html#mechanism-action

Ethozuximide


Lorazepam GABA-A agonist in CNS Dizzines, atazia, drowsiness Website

Diazepam GABA-A agonist in CNS Dizzines, atazia, drowsiness Website

Clonazepam Website

Clobazam

Phenobarbital Sedating

Metabolized to PHB Sedating, Dizziness, Nausea

GABA Reuptake Inhibitors


Nipecotic

Reduces Ca++ currents in thalamus so that the thalamus is the discharge pacemaker.

DOC: Petit Mal; Alternative to Valproic acid

Drugs That Work Via GABA Agonists via increasing GABA prodx, decreasing GABA brkdwn, blocking GABA reuptake, GABA-A agonists

Short TermPartial Szr As IV to terminate szr b/f use of long term AED Absent szr

As IV to terminate szr b/f use of long term AED Absent szr (Short TermPartial Szr

Enhances GABA in Reticular Nucl. Inhibits T-type Ca+ channel currents

Dizzines, atazia, drowsiness Withdrawl may trigger status epilepticus

DOC x Myocloninc Szr & Subcortiical Myoclonis 4th DOC x Absent szr Partial Szr, Panic d/o

Absent szr Partial Szr

Binds to GABA receptor → increase Cl- current, Blocks AMPA receptor, Blocks L and N type Ca++ currents and inhibits Na+ channels

DOC for infants Absent szr Partial Szr

Primidone (metabolized to Phenobarbital)

Partial Szr Absent szr

Tiagabine Inhibits GABA transporter 1 notes

Vigabatrin Inhibits GABA transaminase

GABA Synthesis Inducers


Gabapentin (Neurontin) notes

Pregabalin Incr. GABA in neurons and glial cells notes

Hepatic Toxicity notes

GABA Synthesis Inducers


Felbamate Blocks NMDA receptors Aplastic anemia, SEVERE Hepatitis notes

Topiramate notes

Other AED's


Dizziness, Asthenia, Nrvsness, Tremor, Depression, Emotional Labile

Adjunct thpy x Partial and secondary gen. szr

Absence status drowsiness, (rarely: depression agitation, confusion & psychosis)

DOC x Infantile spasm Used as an adjunct x refactory partial szrs

GABA analog, Decreases GABA metabolism, Inhibits Reuptake

Partial Szr Adjunct Generalized Tonic Clonic Szr (Neuropathic pain, Periperal Neuralgia

Second line adjunct x Partial Szr

Valproic Acid (GABA synth inducer)

At low conc. Blocks voltage Na+ channels. High conc slows influx of Ca++. Increases activity of GABA making enzm (glutamic acid decarbxlylse) and inhibits GABA metabolism.

Generalized Epilepsy Sx. Absence Szr

Partial Szr 3rd line x refractory cases

Inhibits Na+channels from inactive state, incr Cl- flux thru GABA receptors (diff from BZD binding site)

Acute myopia, secondary closed angle Glaucoma, Oligohydrosis, Hyperthermia

Adnunct x Partial Szr & Primary Gen TonClon Szr. Szrs frm LemoxGastut Sx

Progesterone notes

Estradiol notes

notes

Leveritacetum notes

Hypnotics/AnxiolyticsBZDs


Zolpidem GABA receptor agonist (Hypnotic) notes Insomnia

Zaleplon GABA receptor agonist (Hypnotic) Low incidence of rebound insomnia notes Insomnia

Chloral Hydrate Metabolized to Trichloroethanol Tolerance/Dependance notes

Buspirone 5HT1a and DA2 AntAg

Barbs

Clonazepam (BZD) Website

Fluvoxamine SSRI in CNS

Increases GABA channel conductivity, Attenuates glutamate excitatory RE:

PROconvulsant via decreases Cl- flux, and NMDA agonist in hippocampus

CarbonicAnhydrase Inhibitors

Increases intracellular [H+] causing K+ to move out, → hyperpolarization increasing the threshold. (Topiramate, Zonisamide and Acetazolamide)

Daytime sedation; Rebound Insomnia (low);

Anxiety (Atpyical Anxiolytic)

Enhances GABA in Reticular Nucl. Inhibits T-type Ca+ channel currents

Dizzines, atazia, drowsiness Withdrawl may trigger status epilepticus

DOC x Myocloninc Szr & Subcortiical Myoclonis 4th DOC x Absent szr Partial Szr, Panic d/o

Well Tolerated dizziness, HA, insomnia, nervousness, somnolence

ADD/ADHDDrug MOA SDFX Source T(x) For

Methylphenidate DA reuptake inhibitor many PDRDextroamphetamine DA and NE reuptake inhibitor Severe, but in few pts PDRAtomoxetine

Desipramnie

Buproprion 5HT & NE reuptake inhibitor

5HT & NE reuptake inhibitor

Clonidine

Guanfacine A2 agonist HTN

Mood DisordersDrug MOA SDFX Source T(x) For

DA, 5HT & NE reuptake inhibitor notes

Mirtazapine Antidepressant

Nefazodone SSRI (little affinity x alpha adrenergic receptors Antidepressant

5HT & NE reuptake inhibitor

Li effective 50-60% of time Bipolar

Divalporex stabilize temporal lobe Bipolar

Lamotrigine

Topiramate not effective for most ppl BipolarOxacarbamaepine Bipolar

NE reuptake inhibitor, Adenyl cyclase desinsitization, Beta adrenergic receptor downregulation, 5HT receptor downregulation

Antidepressant Smoking cessation

Venlafaxine (and metabolite)

CNS Alpha2 adrenergic Agonist (activating inhibitory pthwys, reducing symp outflow, )

ADD, HTN, Depression

Buproprion (similar strx to amphetamine)

Antidepressant Smoking cessation

TCA alpha2 adrenergic receptor antagonist causing incr NE, 5HT in synapse

sedation, INCREASED appetite (wt gain)

liver failure (death; not used so much anymore)

SNRI (venlagaxine, duloxetine)

Antidepressant, usu more effective

alters ion channel leading to decr in NE, 5HT reuptake

Bipolar reduces cycling and depression NOTHING for mania

CarbamazepineSlows recovery rate of inactive Na+ Channels, preventing the PDS. Metabolite also active. paroxysmal depolarizing shift

Hepatic induction leading to need for MASSIVE dosages. Dizzines, diplopia, nausea, ataxia, blurred vision. Aplatstic anemia, Agranulocytosis, Thrombocytopenia, StvJohnson Sx

Website

Antidepressant DOC: Anticonvulsant (Partial Szr), Anticholinergic, antineuralgic, antidiuretic, muscle relaxant and antiarrhythmic

http://metagenics.com/resources/imc/OneMedicineProf/ProfDrugs/Carbamazepinepd.html#mechanism-action

Gr+Cocci

Anaerobesaerotolerant

StrepEnterococcusStaph

obligatePeptostreoptococcus

BacilliAnaerobes

aerotolerantnonsporforming

LactobacillusCorynebacteriumPropionibacteriumActinomycetesArachniaBacterionema

obligatesporeforming

ClostridiumAerobes

aerotolerantRothia

Gr-Cocci

Aerobes

AnaerobesViellonella

BacilliAnaerobes

aerotolerantnonsporeforming

HaemophilusActinobacillusEikenellaCapnocytophaga

obligateBacteroidesFusobacteriumLeptotrichiaWolinellaSelenomonas

spiral/curvedAnaerobes

aerotolerantCampylobacter

SpirochetesAnaerobes

Neisseria-flavens, mucosa, subflava, meningitidis, sicca

obligateTreponemaBorrelia

Disease Healthy

Test + TP (++) FP (-+)

Test - FN (--) TN (+-)

Disease Healthy

+ Risk Factor

Diseased Pts Exposed (++)

Healthy Pts Exposed (-+)

No Risk Factor -

Disease Pts Not Exposed

(--)

Health Pts Not Exposed (+-)

SyphillisStage Duration Clinical Disease

Incubation None

Primary 8 to 12 weeks Chancre teeming with them

4 to 8 weeks None Inconspicuous

Secondary

Latent None Inconspicuous

Tertiary

Activity of Treponema pallidum

2 to 6 weeks (most often 3 to 4 weeks)

Spirochetes actively proliferate at entry site, spread over body

1. Chancre present at inoculation site

2. Regional lymphadenopathy

Primary Latent

Variable over period of 5 years (Latent periods with recurrences)

1. Skin and mucosal lesions

Skin and mucosal lesions rich in spirochetes (highly infectious)2. Generalized

lymphadenopathy

Few months to a lifetime (average 6 to 7 years)

Variable-rest of patients life

Related to organ system diseased

Paucity of spirochetes in classic lesion

SyphillisDiagnosis Tissue Change

b)Fluorescent antibody

Chancre present

2. STS positive

STS Positive

1. Infection active

2. STS Positive

STS Positive

1. Gumma

2. Special silver stains 2. Healing3. Scarring

4. Tissue distortion

Identification of T. pallidum

Chancre appears at inoculation site

a) Dark-field microscopy

1. Dark-field microscopy of chancre

None demonstrable; Chancre has healed with little scarring

1. Dark-field microscopy

2. Resolution spontaneous

1. STS positive or negative

Actinomycetes

Gr(-) rods. .5>filaments>1mcmtr. Cell wall w/ peptidoglycan, a.a. Streptomyces-are large family of bact. found in soil, H2O, organic debris-primary source for antibiotics.

Etiology Epidemiology Manifestations Treatment Key Diagnostics NotesActinomycosis Normal flora of GI tract, oral cavity.

Cutaneous Infections (Dermatophytosis)Etiology Epidemiology Manifestations Treatment Key Diagnostics Notes

Subcutaneous InfectionsEtiology Epidemiology Manifestations Treatment Key Diagnostics Notes

Systemic InfectionsEtiology Epidemiology Manifestations Treatment Key Diagnostics Notes

Opportunistic InfectionsEtiology Epidemiology Manifestations Treatment Key Diagnostics Notes

General Features

Normal flora of GI tract, oral cavity.

SeizuresGeneralized

Atonic Tonic Clonic Myoclonic Absent

http://pediatricneurology.com/seizure_intro.htm

General Tonic Clonic

SeizuresGeneralized Partial

Simple-No LOC

Complex-+ LOC

Drugs Pharmacology

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