Kaplan internal medicine pdf 2013


 

I'm a admission from Guntur medical college,India and passed out with April 25th and after that,fulltime till my exam date 06/26/ & 06/27/ MTB step3(around times), Archers premier notes(lectures and PDF) the Kaplan Internal medicine boards),repeated mistakes once more and. Kaplan Lecture Notes - Step ruthenpress.info - 2 USMLE Step 3 Lecture. by Kaplan, Inc. Published by Kaplan Medical, a division of Kaplan, Inc. Third F.R.C.S. Clinical Assistant Professor of Surgery Keck School of Medicine, University of . Toronto Psychiatry 55 ruthenpress.info; University of Sharjah; MEDICINE 1 - Fall kaplan lecture notes usmle step 1 brand new packed fully coloured BRS Neuroanatomy 5th Edition pdf Medicine Book, Internal Medicine, Free Ebooks.

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Kaplan Internal Medicine Pdf 2013

Published by Kaplan, Inc. AUTHORS William G. Cvetnic, M.D., M.B.A. history and the clinical 17 ABNORMALITIES OF CHROMOSOMES Trisomy .. The 3 Secrets To Your Bulimia Recovery △△△ ruthenpress.info Certified in Pediatrics and Neonatal-Perinatal Medicine Jacksonville. Kaplan USMLE-1 () - ruthenpress.info Скачиваний: 61 Site Director, Internal Medicine Clerkship and Sub-Internship. Icahn School of. The introduction of DSM-5 in reframed psychiatric nosology, and the reader will find This is the tenth edition of Kaplan & Sadock's Synopsis of Psychiatry to us to USMLE® is a joint program of the Federation of State Medical Boards.

All rights reserved. No part ofthis book may be reproduced in any form, by photostat, microfilm, xerography or any other means, or incorporated into any information retrieval system, electronic or mechanical, without the written permission of Kaplan, Inc. Chapter 1: Fluid Distribution and Edema. Ionic Equilibrium and Resting Membrane Potential. Chapter 2: Chapter 3:

Physical examination shows honey-brown, crusted lesions with an erythematous base on both legs. There are other lesions as well, in various stages of crusting and openness. The examination is otherwise normal. Differential Diagnosis 1. Impetigo 2.

Cellulitis 3. Erysipelas Varicella Folliculitis S. The presence of lesions on exposed legs the patient wore short pants and walking outside in the woods suggest some form of problem secondary to contact. Skin lesions due to staphylococcal infections are more likely to occur at the base of follicles and will range from papulovesicular to bullae. There is no evidence of any deeper or more widespread disease, such as cellulitis, erysipelas, or staphylococcal scalded skin syndrome.

Patients with staphylococcal scalded skin appear much more toxic. Over-the-counter combinations of bacitracin-neomycin-polymixin B are less effective. Oral treatment is warranted if there are widespread lesions or bullous lesions. If methicillin-resistant S. Vancomycin is not recommended for oral use but is highly effective intravenously, especially for MRSA.

Discussion A summary of vesicles and bullae is as follows. With touch or pressure, skin will easily exfoliate. Follow-up Management and Prevention Typically, 7 days of therapy is sufficient for mild cases.

Crusted lesions may be washed gently. Scratching can spread the organism. She denies eye pain and does not recall any trauma to the eye. Physical examination reveals diffuse conjunctival hyperemia of the left eye associated with a mucoid discharge and pupils that dilate normally with mild photophobia in the affected eye.

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There is no adenopathy. The funduscopic examination, eye movement, and visual acuity are all normal. Always consider N. Unilateral versus bilateral erythema is a good first step in thinking about the differential diagnosis. Viral conjunctivitis is likely to be bilateral with a watery discharge.

Allergic conjunctivitis should have itchiness, be bilateral and watery, and have a seasonal component and perhaps other history of allergic disease. With no history of pain or trauma caused by a foreign body, chemical conjunctivitis or corneal abrasion is highly unlikely. Normal vision and no ophthalmoplegia or proptosis, normal and symmetric pupillary size and reaction rule out anterior uveitis, orbital cellulitis, and glaucoma. Perform fundoscopic examination.

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However, it is most commonly treated with a topical ophthalmic antibiotic. Discussion Neonatal red eye With eye drainage: perform Gram stain and culture for N. Orbital cellulitis is an emergent condition and needs immediate referral to ophthalmology.

MRI of the orbit and surrounding tissue should be performed to aid surgical drainage.

Kaplan Internal Medicine Lecture Notes, ( 2014)

Start IV antibiotics immediately. Final Diagnosis Bacterial conjunctivitis CASE REVIEW Bacterial Conjunctivitis Red eye with discharge History of crusting Typically painless Topical antibiotic treatment Viral Conjunctivitis Associated with upper respiratory infection 20 Look for clear discharge Glaucoma Painful, blepharospasm, tearing, megalocornea Abnormal pupil response Ophthalmologist consultation necessary Corneal Abrasion Painful Photophobia Trauma with abrasion Fluorescein stain for corneal abrasion Prophylactic topical antibiotics Uveitis Painful Visual disturbances Abnormal pupils Slit lamp examination: inflammatory cells in anterior chamber Treat underlying disease with or without topical steroids 21 Case 2 Chief Complaint Rash on legs History and Physical Examination A 6-year-old boy is brought to the office because of a rash that started as a superficial accumulation of several small vesicles on his legs below the knees.

There is no fever or chills. He lives in the suburbs and often walks outside in the local woods in short pants.

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Vital signs are T Ions move across the membrane via channels see below. Net force driving force. It is estimated by subtracting the ions equilibrium potential from the cell's membrane potential.

In short, it quantitates how far a given ion is from equilibrium at any membrane potential. Figure 11 - 1 - 1. Basic Schematic of an Excitable Cell.

Ions diffuse across the membrane via ion channels. There are 3 basic types ofion channels Figure II Figure 11 - 1 - 2. Classes of Ion Channels. Above, we defined the 3 basic classes into which ion channels fall The. Figure 11 - 1 - 3. NMDA Receptor. Glutamate and aspartate are the endogenous ligands for this receptor. Binding of one ofthe ligan"ds is required to open the channel, thus it exhibits characteristics of a ligand-gated channel. Thus, opening ofthis channel results in depolarization.

Although the NMDA receptor is likely involved in a variety offunctions, the 2 most important are 1 memory and 2 pain transmission. With respect to memory, NMDA has been shown to be involved in long-term potentiation of cells, thought to be an important component ofmemory formation. Thus, opening of ion channels does not alter intracellular or extracellular concentrations of ions under normal circumstances. The following representreasonableequilibrium potentialsfor the key electrolytes:.

Eel- - mV. In depolarization, Em becomes less negative moves toward zero. There is marked variability in the resting membrane potential rEm for excitable tissues, but the following generalizations are applicable. If acute, excitability of nerves is increased nerve is closer to threshold for an action potential and heart arrhythmias may occur. This decreases the excitability of nerves further from threshold and heart arrhythmias may occur.

Recall that increasing g for an ion causes the Em to move toward the equilibrium potential for that ion. Thus, the cell will move from mV toward mV. Figure 11 - 1 - 4. Thus decreasing g or changing the extracellular concentration has no effect on rE m. The NMDA receptor is the exception, because it is both ligand and voltage-gated.

The action potential is a rapid depolarization followed by a repolarization return of membrane potential to rest.

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The function is:. Figure Il shows the action potential from 3 types of excitable cells. Even though there are many similarities, there are differences between these cell types, most notably the duration of the action potential. In this chapter, we discuss the specific events pertaining to the nerve action potential, but the action potential in skeletal muscle is virtually the same. Thus, what is stated here can be directly applied to skeletal muscle.

Figure 11 - 2 - 1. Action Potentials from 3 Vertebrate Cell Types. Redrawn from Flickinger, C. Medical Cell Biology, Philadelphia, , W.

Saunders Co. The opening of these channels is responsible for the rapid depolarization phase upstroke of the action potential. It has 2 gates and 3 conformational states:.

However, because of the slow kinetics, a period of hyperpolarization occurs. Occurs if threshold is reached, doesn't occur if threshold is not reached. Figure 11 - 2 - 4.

AxonAction Potential and Changes in Conductance. Under normal circumstances, an action potential in the motor neuron releases enough Ach to cause an EPP that is at least threshold for the action potential in the skeletal muscle cell.

The actions of Ach are terminated by acetylcholinesterase AchE , an enzyme located on the postsynaptic membrane that breaks down Ach into choline and acetate. Outside ofthe CNS, these primarily reside in autonomic ganglia. Muscarinicreceptorsare G-proteincoupledreceptors.

These resideintarget tissues innervated by parasympathetic postganglionic neurons. Figure II illustrates synaptic junctions between neurons. Botulin um toxin is a protease that destroys proteins needed for the fusion and release of synaptic vesicles. This toxin targets cholinergic neurons, resulting in flaccid paralysis. Many pesticides, as well as some therapeutic agents, blockAchE, resulting in the prolonged action ofAch in cholinergic synapses. N M receptors non-depolarizing neuromuscular blockers , while succinylcholine binds to this receptor causing the channel to remain open depolarizing neuromuscular blocker.

Two important pathologies related to neuromuscular junctions are. The most common form of myasthenia gravis is an autoimmune condition in which antibodies are created that block the N M receptor.

These are clinical signs intended to help further reinforce the important physiology and thus aid the student in recognizing possible causes of these clinical signs. Clinical signs could include: Possible causes include the following. Step 1 Physiology Lecture Notes. Contents Preface. Fluid Distribution and Edema Chapter 1: ExcitableTissue Chapter 1: Skeletal Muscle Chapter 1: Section VIII: Gastrointestinal Physiology Chapter 1: Kaplan Medical. Explanations Figure The 2 primary regulators of ADH are: The 3 primary regulators of renm are: Starling Equation These 4 forces are often referred to as Starling forces.

Grouping the forces into those that favor filtration and those that oppose it, and taking into account the properties of the barrier to filtration, the formula for fluid exchangeis the following: Lymphatics The lymphatics play a pivotal role in maintaining a low interstitial fluid volume and protein content.

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