RA onset is usually insidious, often beginning with systemic nonspecific symptoms and joint symptoms.

• Nonspecific signs & symptoms (last for weeks/months), include: fever, malaise, arthralgias, and weakness.

The disease progresses most rapidly during the first 6 yr, particularly the first year; 80% of patients develop some permanent joint abnormalities within 10 yr. The course is unpredictable in individual patients.

• Specific signs and symptoms that take weeks to months to appear.

Joint symptoms are characteristically symmetric, include:

– Stiffness lasts > 60 minutes after rising in the morning but may occur after any prolonged inactivity (called gelling).

– Erythema, warmth, swelling, and limitation of motion.

Joints involved in rheumatoid arthritis, include

The most common joints involved are;

1. Wrists and
2. the index (2nd) and middle (3rd) metacarpophalangeal (MCP) joints

Other joints include;

1. Proximal interphalangeal (PIP) joints
2. Metatarsophalangeal (MTP) joints
3. Shoulders
4. Elbows
5. Hips
6. Knees
7. Ankles

Any joint, except the distal interphalangeal (DIP) joints can be affected.

Irreversible Joint Deformities may occur due to disease progression. They include:

1. Ulnar deviation of the fingers
2. Boutonniere Deformity (hyperextension of the DIP & flexion of the PIP joint)
3. Swan Neck Deformity (hyperextension of the PIP & flexion of the DIP joint)

Extra-articular Manifestations

RA is a systemic disease that involves other organs. Most of rheumatoid arthritis extra-articular manifestations are collected in this image related to the involved organ.

Subcutaneous rheumatoid nodules develop in 20% of patients, usually at sites of pressure and chronic irritation (eg, the extensor surface of the forearms, elbows, hands, and feet).

Other extra-articular manifestations of RA are included in the image.

We hope this part of the map make it easier for you to study RA clinical presentation. And till our next post, study smart not hard and don’t hesitate to send us your questions.

If you’re interested in getting this map, please check out our Store.

Definition:

Each word in the definition makes a link to a piece of information about rheumatoid arthritis (RA);

• RA is a chronic inflammatory autoimmune disease —(this takes you to disease’s etiology & pathophysiology),
• It involves the joints and may cause systemic manifestations —(this takes you to RA signs and symptoms and extra-articular manifestations)

Etiology:

RA is an autoimmune disease with unknown cause. Although, some contributing factors (genetic & environmental) may be involved. For example, environmental factors (e.g, viral infections, cigarette smoking) trigger and maintain joint inflammation.

Pathophysiology:

The image shows a simplified hierarchy for the pathophysiology of rheumatoid arthritis.  Although, the pathogenesis of RA is not completely understood, it is theorized that external trigger (e.g, cigarette smoking, infection, or trauma) along with hereditary predisposition triggers an autoimmune reaction, leading to chronic joint inflammation of the synovial tissue ending with joint destruction with the potential for extra-articular manifestations.

This moves us to the following point which is RA clinical presentation (on our next post). Till the next post, study smart not hard and share this part of the map with your colleagues.

To order the full map, please visit our shop.

This moves us to the following point which is RA clinical presentation (on our next post). Till the next post, study smart not hard and please don’t hesitate to send us your questions.

Rheumatoid Arthritis Concept Map: An Overview

You can access this map for free. But if you want it as a printable version or a folded poster, please order here.

Etiology and Pathophysiology of Rheumatoid Arthritis

Most of rheumatoid arthritis extra-articular manifestations are collected in this image:

Rheumatoid arthritis extra-articular manifestations

Diagnosis

 This part of the map includes: History and Examination – Laboratory tests – Radiographic test (x-ray) – ACR Rheumatoid Arthritis Diagnostic Criteria (2010). In addition, a comparison between rheumatoid arthritis and osteoarthritis is included.

Rheumatoid Arthritis vs Osteoarthritis

Treatment

– adverse effects: GI toxicity, headache, confusion and other CNS symptoms, increased BP, worsening of hypertension, edema, and decreased platelet function. NSAIDs increase cardiovascular risk.

Non-steroidal anti-inflammatory drug drugs mechanism of action is shown in this diagram:

Non-steroidal Anti-inflammatory Drugs – Mechanism of Action

• adjunctive therapy
• decrease inflammation and other symptoms rapidly and efficiently
• slow bone erosion

When to use low-dose systemic CS in RA?

• In early RA, low-dose oral prednisone (<10mg/day) in combination with DMARDs for up to 6 months, as symptomatic effects ↓ with time
• In established RA, CS may be used as ‘bridging’ therapy when DMARDs are initiated, and should be withdrawn once
  DMARDs have controlled the disease
• May be used for severe joint or systemic manifestations of RA (eg, vasculitis, pleurisy, pericarditis)

Contraindications

• Relative contraindications include PUD, HTN, untreated infections, DM, and glaucoma
• The risk of latent TB should be considered before CS therapy is begun

• Early treatment of RA (< 6 months after the onset of symptoms) with DMARDs retard disease progression more efficiently and induce more remissions.
• Until the full action of DMARDs takes effect, anti-inflammatory or analgesic medications may be required as bridging therapy to reduce pain and swelling.
• They differ from each other chemically and pharmacologically.
• Patients should be informed about the risks of DMARDs and monitored closely for evidence of toxicity.
• Combinations of DMARDs may be more effective than single drugs. Also, combining a DMARD with another drug, such as methotrexate plus a TNF-α antagonist or an IL-1 receptor antagonist or a rapidly tapered corticosteroid, may be more effective than using DMARDs alone.

A comparison between DMARDs is available in the map. The comparison is showing: mechanisms of actions, indications, doses, adverse effects, monitoring parameters, and contraindications.

• Also called “biologic DMARDs”
• They are not given in combination with each other due to increased frequency of infections.
• Approved by the FDA to treat moderate to severe RA not responded to an one or more of the traditional DMARDs
• They may be used alone, but are often in combination with other DMARDs, to increase the efficacy and decrease AE
• Start biologic agents while patients remain on NSAID and/or corticosteroid

A comparison between biologic agents is available in the map. The comparison is showing: mechanisms of actions, indications, doses, onset of action, adverse effects, contraindications, and warnings/cautions.

• Efficacy is similar to DMARDs but more toxic.
• Used in case of treatment failure with DMARDs or to ↓ the need for CSs.
• Used infrequently unless there are extra-articular complications.

And here is a comparison between them:

We hope you find Rheumatoid Arthritis Concept Map helpful.  Please let us know your opinion in a comment below. You can access this map for free. But if you want it as printable version or a folded poster please order below.

Diabetes Mellitus – Criteria for diagnosis and diagnostic tests

Symptoms of hyperglycemia are written under (DIAGNOSIS), where DM diagnostic criteria. DM is diagnosed by demonstrating any one of the following along with symptoms of hyperglycemai:

Treatment of DM type 1 includes : insulin, diet, and exercise, while treatment of type 2 includes: diet, exercise, oral antidiabetics (OAD), insulin.

Type 1 Diabetes Mellitus vs Type 2

Diabetes Mellitus – Pathophysiology and treatment map (abbreviations are mentioned in the map)

Diabetes Mellitus Complications – Diabetic ketoacidosis (DKA)

Lifelong insulin is required in all type 1 DM patients and it should be started immediately after diagnosis, unless patient probably will experience an acute complication of diabetes which is called “Diabetic Ketoacidosis” – DKA.  It is a diabetic emergency that is caused by absolute or relative insulin deficiency.  A separate concept map for diabetic ketoacidosis is included to give an overview of DKA definition, pathophysiology, diagnosis, and management.  Next to DKA map, there is an overview of another diabetic complication called “Hyperosmolar Hyperglycemic State” – HHS which mainly occurs in type 2 DM patients. Differences between DKA and HHS are highlighted with dotted boxes.

Diabetes Mellitus Folded Map

This map is available in two forms: printable version and folded poster. We hope you find Diabetes Mellitus Concept Map helpful and we are looking forward to hearing your opinion.

References

“Diabetic Ketoacidosis (DKA).” The Merck Manuals for Healthcare Professionals. May 2007. Merck Medicus. 29 April 2009 DiPiro, Joseph T. Pharmacotherapy: A Pathophysiologic Approach. 8th. The McGraw-Hill Companies , 2011. Fauci, Anthony S., et al. Harrison’s Online. 17th Edition ed. The McGraw-Hill Companies, 2008. Merck Medicus. 2008. 17 Feb. 2009 <http://www.merckmedicus.com/pp/us/hcp/frame_textbooks.jsp?pg=http://www.accessmedicine.com/resourceTOC.aspx? resourceID=4>  // //

What is Parkinson Disease (PD)?

Part of Parkinson Disease (PD) Concept Map – definition, epidemiology, etiology, and signs and symptoms

1. Smaller handwriting (micrographia)
2. Infrequent blink
3. Excessive drooling (sialorrhea) may contribute to disability
4. Soft voice trails off
5. Speech becomes hypophonic, … etc.

Parkinson Disease Differential Diagnosis

• Common features of atypical parkinsonism that differentiate it from PD.
• Forms of atypical parkinsonism and associated conditions.

Parkinson disease vs atypical parkinsonism – PD differential diagnosis Zoom-out-pharmacotherapy

the substantia nigra pars compacta (SNc), causing the motor manifestations of PD. This point leads you to understand first the role of dopamine and dopamine metabolism in disease’s pathophysiology and treatment.

Part of Parkinson Disease Concept Map – Pathophysiology and Treatment of Parkinson Disease

Parkinson’s Treatment

Dopamine metabolism and Antiparkinson drugs mechanisms of actions Order the full map

This part of the map links between dopamine metabolism in presynaptic neurons and antiparkinson drugs mechanisms of actions. Pharmacological treatment of PD aims to restore dopaminergic function in the brain using one or more of the following:

• Carbidopa/L-Dopa
• COMT Inhibitors
• MAO-B Inhibitors
• DA Agonists
• Anticholinergic Medications
• Amantadine

For each drug or drug class, its mechanism of action, efficacy against PD symptoms, adverse effects, precautions or drug interactions if present are explained.

It is important to state that treatment of PD doesn’t prevent progression of the disease and drug choice is based on symptoms. For example, Levodopa is most effective at relieving bradykinesia and rigidity, although it often substantially reduces tremor. On the other hand, anticholinergic medications are effective against IPD tremor in about 50% of patients; not bradykinesia or rigidity.

Antiparkinson Drugs Table Comparisons

Beside using the way of concept mapping to build information upon each other (information about drugs mechanisms of action and indications are built upon dopamine metabolism), there are also table comparisons for antiparkinson drugs. There are three tables that compares:

1. Catechol-O-methyl transferase inhibitors (COMT inhibitors): Tolcapone and Entacapone.
2. Monoamine oxidase B inhibitors (MAO-B inhibitors): Selegiline and Rasagiline
3. Nonergot dopamine agonists: Apomorphine, Pramipexole, Ropinirole, and Rotigotine transdermal.

Antiparkinson drugs table comparisons

L-dopa motor complications

Despite its efficacy as a symptomatic treatment of Parkinson disease, long-term L-dopa therapy is associated with disabling motor complications. These complications includes:

1. End-of-dose wearing off (motor fluctuation)
2. “Delayed-on” and “no-on” response
3. Freezing
4. Dyskinesias
5. “Off-period” dystonia

These complications are represented in the map through a table that contains clinical features, mechanism, and management approach for each of l-dopa motor complications.

Levodopa motor complications table – clinical features, mechanism, and management

Surgical Management of Parkinson Disease

Surgical Management of Parkinson Disease

Surgery should be considered as an adjunct to pharmacotherapy in case that PD symptoms not adequately controlled with optimized medical therapy. The map briefly states surgical procedures for the treatment of PD, including the most common procedure which is Deep brain stimulation (Thalamic Stimulation) and its patient selection criteria.

Management of Special Situations

Hallucination and  cognitive disorders associated with PD

Parkinson disease is associated with nonmotor symptoms that may be caused by either the disease itself or the anti-parkinson drugs. These nonmotor symptoms can be hallucinations/psychosis, cognitive disorders, sleep disorders, depression, agitation, anxiety, constipation, orthostatic hypotension, seborrhea, and blepharitis. The goal in the management of Parkinson disease is to improve motor and nonmotor symptoms

in order to improve quality of life. This part of the map gives and overview about medications that can be used in the management of nonmotor complications and those that should be avoided in order not to worsen Parkinson symptoms.

This map is available in two forms: printable version and folded poster. We hope you find Parkinson Disease (PD) Concept Map helpful.  

Parkinson Disease (PD) Concept Map by Maha Atef, B Pharm, PGDip (ClinPharm), PGDip (TQM).

Last updated on:  26 October 2014

Obesity Concept Map: An Overview

The aim of this concept map is to clarify the approach for evaluating and managing overweight/obesity patients.

Definition

Etiology and Risk Factors

• Genetic factors; cause primary obesity
• Environmental factors
• Secondary causes; medications and medical conditions that may cause secondary obesity
• Psychiatric disorders
• Physiological factors
• Other risk factors

Obesity Etiology and Risk Factors – part of the map

Classification

• Primary obesity
• Secondary obesity

Classification of obesity according to BMI

According to waist-to-hip ratio

• Apple obesity
• Pear obesity

Diagnosis and Clinical Presentation

Complications and Comorbidities

Treatment of Obesity

Obesity Folded Map

This map is available in two forms: printable version and folded poster. We hope you find Obesity concept map helpful and we are looking forward t hearing your opinion.

Here is an overview about our unique “One Picture” on Drug-drug interactions (DDIs) concept map from Zoom out – Pharmacotherapy. Although this map comes into two large pictures; one for Pharmacokinetic drug interactions and the other is for Pharmacodynamic drug interactions.

More about this map is found on our website. Please visit Drug-Drug Interactions Concept Map page.

Types

Pharmacokinetic Interactions

Absorption Interactions

• Drug Binding

• Changes in Gastrointestinal Motility

• Alteration in Gastrointestinal pH

• Effect on Intestinal Flora

Effect of intestinal flora – Absorption drug interactionsClick to enlarge

• Alterations in Drug Metabolism within the Intestinal Wall

Hypertensive crisis caused by co-administration of tyramine containing food with MAO inhibitors is a clinically significant drug interaction that is shown as an example in this part of the map.

Alteration in drug metabolism within the intestinal wallClick to enlarge

Distribution Interactions

1. Displacement.
2. Drug-induced decrease in concentration of binding protein.

Metabolism Interactions

Many administered drugs are extensively metabolized in the liver by hepatic enzymes. The most common among these enzymes are cytochrome P450 enzymes. Know about these enzymes’ nomenclature, function and other information through this part of the map.

Cytochrome P450 nomenclature and function Click to enlarge

Cytochrome P450 drug-drug interactions can occur through:

• Enzyme Inhibition

CYP450 enzyme inhibition mechanism

You’ll also find a table with some examples of interacting drugs through inhibition of cytochrome P450 enzymes.

• Enzyme Induction

CYP450 enzyme induction mechanism

There is also a table with some examples of interacting drugs through inhibition of cytochrome P450 enzymes.

Effect of CYP450 inhibitors and inducers on prodrugsClick to enlarge

Excretion Interactions

• Glomerular Filtration

• Active Tubular Secretion

• Passive Tubular Reabsorption

Passive tubular reabsorption – Excretion drug interactionsClick to enlarge

Then, know how urine alkalinization results in more reabsorption of basic drugs and increases the excretion of acidic drugs as methotrexate to prevent or reverse drug toxicity.

Pharmacodynamic Interactions

Mechanisms of Pharmacodynamic Interactions

1. Additivity
2. Synergism
3. Antagonism

Don’t miss this table – #Antibiotic Therapy in #Urinary_Tract_Infections

The table shows different types of urinary tract infections (Cystitis, Uretheritis, Acute urethral syndrome, Epididymitis, Acute pyelonephritis, and Bacterial Prostatitis) with the recommended antibiotic therapy regimen and duration of therapy.

The whole map is available for free on www.zoomout-ph.com/2012/02/urinary-tract-infection-mind-map.html

I hope you find it useful and I look forward knowing your opinion.

• What is depression?
• What causes depression?
• What are the signs and symptoms of depression?
• Non pharmacological treatment for depression
• Pharmacological treatment of depression

• Major depressive disorder /Major depression / Unipolar depression
• Dysthymia
• Postpartum Depression
• Seasonal Affective Disorder (SAD)
•  Depressive disorder not otherwise specified
•  Mixed anxiety-depression

Phathophysiologic Hypotheses of Depression – Click on the image to enlarge

•  how antidepressants work (i.e. mechanisms of action) and
• what adverse effects they produce 

• exclude bipolar depression; as major depression is a unipolar disorder.
• exclude general medical illness, drug therapy, or substance abuse, that is why patients should undergo physical examination, mental status examination, basic laboratory work-up (CBC, thyroid function tests, and electrolyte determinations).
• determine depression case severity using psychometric rating instruments as Hamilton Psychiatric Rating Scale for Depression (HAMD)

• Psychotherapy could be the first-line therapy in mild to moderate depression, but not used alone in case of acute severe and/or psychotic major depressive disorder.
• Electroconvulsive Therapy (ECT) is safe and effective for severe mental illnesses, including all subtypes of major depression.  It is reserved for treatment-resistant cases and delusional depressions.
• Light therapy.

• Selective Serotonin Reuptake Inhibitors (SSRIs): citalopram, escitalopram, fluoxetine, fluvoxamine,
  paroxetine, and sertraline
• Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs): duloxetine, venlafaxine, desvenlafaxine
• Norepinephrine-Dopamine Reuptake Inhibitors: Bupropion only
• Tricyclic Antidepressants (TCAs) and Other Heterocyclics: amitriptyline, imipramine, nortriptyline, desipramine, amoxapine
• Serotonin Modulators (5-HT2 blockers): nefazodone and trazodone
• Alpha-2 Antagonist: Mirtazapine
• Monoamine Oxidase Inhibitors (MAOIs): phenelzine, isocarboxazid, and tranylcypromine → nonselective (inhibit MAO-A and MAO-B), selegiline (transdermal patch) → inhibits only MAO-B at lower doses
• St. John’s.

This map is available in two forms: printable version and folded poster.We hope you find Depression Concept Map helpful and we are looking forward to hearing your opinion.

Depression Concept Map by Maha Atef, B Pharm

Last updated on: 13 June 2012

Back to Diseases and Conditions

// //

Although depression is a disorder of unknown cause, many hypotheses have tried to explain the pathophysiology of depression.  Among the most prominent of these hypotheses are those mentioned in the following map of (Phathophysiologic Hypotheses of Depression):

The first one is “Catecholamines Hypothesis” which proposes that depression is linked to decreased brain levels of the neurotransmitters norepinephrine (NE), serotonin (5-HT), and/or dopamine (DA).  But it has been observed that the administration of antidepressants causes immediate increase in the synaptic levels of monoamines (NE and 5-HT)producing antidepressants adverse effects, while the antidepressive effects are not observed until after few weeks of dosing.  That observation is explained by the second hypothesis which is (Receptor Sensitivity Hypothesis).

•  how antidepressants work (i.e. mechanisms of action) and
• what adverse effects they produce

I hope you gain value from this map, and I look forward to hearing your feedback.