Zoom out Contest (SAVE 60%)

Zoom out - Pharmacotherapy Contest - SAVE 60%
Zoom out – Pharmacotherapy Contest

We’ve a great offer for you!
We challenge you to answer 6 Questions correctly, then you’ll be able to get a gift coupon code and SAVE 60% of the price of any 6 maps you choose.

Now, go to contest form; answer the 6 questions and submit them before 16th of December 14.

——————–

This contest is not available now. You can check the answers and the corresponding parts of the maps through this link on our Website.

http://www.zoomout-ph.com/2014/12/zoom-out-contest-answers-from-parts-of.html

Rheumatoid Arthritis (RA) Clinical Presentation

Our dear readers, we’re still focusing on Rheumatoid Arthritis (RA) Concept Map. And here is new part of the map; it is related to Rheumatoid Arthritis Clinical Presentation.

Rheumatoid Arthritis Clinical Presentation - Part of RA Concept Map
Rheumatoid Arthritis Clinical Presentation – Part of RA Concept Map – Click on image to enlarge

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.

RA signs and symptoms -  Part of RA Concept Map
RA signs and symptoms – Part of RA Concept Map – Click on image to enlarge

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.

Extra-articular Manifestations of Rheumatoid Arthritis
Extra-articular Manifestations of Rheumatoid Arthritis

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.

Rheumatoid Arthritis Definition, Etiology, and Pathophysiology

Dear followers, we’d like to invite you to check our blog for the coming few days; we’ll post about Rheumatoid Arthritis (RA) and how to study it as one unit through our map. The aim of this is to make it easier for you to study the disease through a meaningful way of learning. This way is based on building information upon each other and drawing logical links between it.  Are you ready?! Then, open Rheumatoid Arthritis Concept Map and follow our posts.

Rheumatoid Arthritis (RA) Definition, Etiology, Pathophsiology, and More
Rheumatoid Arthritis (RA) Definition, Etiology, Pathophsiology, and More

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 (RA) Concept Map

Rheumatoid Arthritis Concept Map
Rheumatoid Arthritis Concept Map – Click to enlarge image

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.

Definition

Rheumatoid Arthritis is a chronic inflammatory autoimmune disease that involves the joints and may cause systemic manifestations.

Etiology

It is an autoimmune disease with unknown cause. Some contributing factors (genetic & environmental factors) may be involved in the disease. Environmental factors like: viral infections and cigarette smoking; trigger and maintain joint inflammation.

Epidemiology

– Prevalence; 1% worldwide
– Gender; Women : Men = 3:1 (after 50 years old, gender difference is less marked)
– Age; peaks at 35-45 years old, although it can occur at any age – when it occurs in childhood, it is called “Juvenile Idiopathic Arthritis”
– Limitations of activities:
     * 33% have major activities limited
     * 29% cannot perform major activities

Pathophysiology

Rheumatoid arthritis pathophysiology is shown in the map in the form of a cascade process that starts by an “Autoimmune
Reaction” and ends by “Joint Destruction.”
Etiology and Pathophysiology of Rheumatoid Arthritis
Etiology and Pathophysiology of Rheumatoid Arthritis

Clinical Presentation

Nonspecific signs & symptoms (for weeks/months): fever,malaise,arthralgias, and weakness
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;
         Wrists, feet (MTP), and the index (2nd) and middle (3rd) metacarpophalangeal (MCP) joints
Other joints include;
         Proximal interphalangeal (PIP) joints, shoulders, elbows, hips, knees, and ankles.
Any joint, except the distal interphalangeal (DIP) joints

Irreversible Joint Deformities may occur due to disease progression

  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)
  4. Hammer toe deformity
Progression
Disease progresses most rapidly during the first 6 years, particularly the first year; 80% of patients develop some permanent joint abnormalities within 10 years.

Extra-articular Manifestations

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

Rheumatoid arthritis extra-articular manifestations
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
Rheumatoid Arthritis vs Osteoarthritis

Treatment

Treatment goals for rheumatoid arthritis are linked to medications used in managing the diseases.

Medications to Reduce Pain and Inflammation

1) Non-Steroidal Anti-inflammatory Drugs (NSAIDs)

e.g., ibuprofen, naproxen, ketoprofen, piroxicam, and diclofenac
– adjunctive therapy
– treat symptoms and decrease inflammation  but do not affect disease progression.
– dose can be decreased or discontinued with successful Disease-modifying antirheumatic drugs (DMARDs) therapy.

– 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
Non-steroidal Anti-inflammatory Drugs – Mechanism of Action

2) COX-2 inhibitor (only celecoxib)

See the map.

3) Low-dose systemic corticosteroids (CS)

  • 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

4) Intraarticular depot corticosteroids

– Temporarily control severe monarticular or even oligoarticular symptoms
– Triamcinolone hexacetonide may suppress inflammation for the longest time
– Triamcinolone acetonide and methylprednisolone acetate are also effective
– No single joint should be injected with a corticosteroid more than 3 to 4 times a year, as too-frequent injections may accelerate joint destruction
– Because injectable corticosteroid esters are crystalline, local inflammation transiently increases within a few hours in < 2% of patients receiving injections
– Although infection occurs in only <1:40,000 patients, it must be considered if pain occurs > 24 h after injection

Medications to Prevent Disease Progression & loss of joint function

1)     Disease-modifying antirheumatic drugs (DMARDs)

Also called “nonbiologic DMARDs,” include: methotrexate (MTX), hydroxychloroquine (HCQ), azathioprine (AZA),
sulfasalazine (SSZ), and leflunomide.
Other available but rarely used DMARDs include minocycline, azathioprine, cyclosporine, and tacrolimus.
  • 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.

Disease Modifying Anti-Rheumatic Drugs (DMARDs) - Table Comparison - Zoom out - Pharmacotherapy
Disease Modifying Anti-Rheumatic Drugs (DMARDs) – Table Comparison

2)     Biologic Agents

  • 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.
Biologic DMARDs - Table Comparison - Zoom out - Pharmacotherapy
Biologic DMARDs – Table Comparison

3)     Other immunomodulatory, cytotoxic, and immunosuppressive drugs

e.g., Azathioprine, and cyclosporin A.  Rarely cyclophosphamide and d-Penicillamine
  • 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:

Other immunomodulatory, cytotoxic, and immunosuppressive drugs - Table Comparison - Zoom out - Pharmacotherapy
Other immunomodulatory, cytotoxic, and immunosuppressive drugs – Table Comparison

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.

Rheumatoid Arthritis concept map by Maha Atef, B Pharm.

Version: 2.0

Last updated in: 10 June 2014

Diabetes Mellitus Concept Map

diabetes mellitus concept map from Zoom out - Pharmacotherapy
Diabetes Mellitus Concept Map Order the full map

Definition

The map starts with Diabetes Mellitus (DM) definition which is a syndrome that is caused by absolute or relative lack of insulin, resistance to the action of insulin, or both.  It is characterized by hyperglycemia and alteration in lipid and protein metabolism. This definition is linked with the normal physiology of insulin and glucagon secretion in response to blood glucose level (BGL).  From DM definition, there are also links to symptoms of hyperglycemia and DM complications (including micro- and macrovascular complications).

Diagnosis

Diabetes Mellitus - Criteria for diagnosis and diagnostic tests
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:

  • Symptoms of hyperglycemia or hyperglycemic crisis plus casual plasma glucose ≥ 200 mg/dL (11.1 mmol/L)
  • Fasting plasma glucose ≥ 126 mg/dL (7.0 mmol/L)
  • 2-hour postload glucose ≥ 200mg/dL (11.1 mmol/L) during OGTT
  • HbA ≥ 6.5%.
From these criteria, there are links to DM diagnostic tests including: Random Blood Glucose Test, Fasting Blood Glucose Test, Oral Glucose Tolerance Test (OGTT)/2-Hour Postprandial Test, and Glycosylated Hemoglobin (HbA1C), with a comparison of their relevant values of blood glucose level in cases of normal BGL, Impaired glucose tolerance (IGT), Impaired fasting glucose (IFG), Increased risk of diabetes mellitus, and values in case of DM.

Monitoring

Although (MONITORING) part is usually mentioned in any reference at the end of the topic, it is mentioned in this map close to (Diagnosis) part to show differences between all tests used in diabetes and to clarify which ones that are used for diagnosis and/or monitoring. Tests that are used in DM monitoring are: Self / Home Monitoring of Blood Glucose (SMBG /HMBG), Glycosylated Hemoglobin (HbA1C), and Serum Fructosamine.  Each one is explained and followed by normal values of BGL and values that indicate DM or inadequate glucose control.  (Monitoring) part is also followed by explanations of screening tests that are usually used by diabetic patients.  The first one is screening for glucose in urine, a condition that is called (Glucosuria) and the second is to screen for ketones in urine, a conditions that is called (Ketonuria). The other part of (Monitoring) is related to DM complications, when to start monitor for these complications and what monitoring tests are used.

Types of Diabetes mellitus

comparison between diabetes mellitus type 1 and type 2 is included within the map.  This comparison covers the following points:
Age of onset – Onset – Risk Factors -Pancreatic Function – Pathophysiology – Clinical Presentation – Obesity – Complications – Treatment.

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 - comparison
Type 1 Diabetes Mellitus vs Type 2

Treatment

A mind map of diabetes mellitus treatment is included under (TREATMENT). The main function of this map is to differentiate between the sites of action of medications used in the management of DM, i.e. to show whether this medicine acts to stimulate pancreatic insulin secretion (Insulin secretagogues), decrease  peripheral insulin resistance (Thiazolidinediones), decrease hepatic glucose production (Biguanides), or slow digestion and absorption of carbohydrates (α-Glucosidase inhibitors (AGIs)) …etc.  Medications used in the management of diabetes mellitus are discussed in comparisons that involve their mechanisms of action, adverse effects, drug interactions, precautions, and contraindications if any.
Diabetes Mellitus - Pathophysiology and treatment map
Diabetes Mellitus – Pathophysiology and treatment map (abbreviations are mentioned in the map)

The pharmacological treatment of diabetes mellitus includes:

  • Insulin
  • Glucagon-Like Peptide 1 (GLP-1 ) Agonists (Incretin mimetics )
  • Oral Antidiabetics (OAD)
  • Insulin secretagogues:

1) Sulfonylureas (SU’ s) / Long-acting insulin secretagogues 2) Meglitinides / Short-acting insulin secretagogues

  • Insulin sensitizers

1) Biguanides 2) Thiazolidinediones (TZDs) / Glitazones / PPARγ Agonists

  • Intestinal enzyme inhibitors

α-Glucosidase inhibitors (AGIs)

  • Dipeptidyl peptidase – 4 inhibi tors
  • New therapies:

–          Amylin analogue –          Dopamine Agonists –          Bile Acid Sequestrants

 Diabetes Complications

Diabetes Mellitus Complications - Diabetic ketoacidosis (DKA) - diagram
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.

Patient education icon is scattered at different sites within the map to indicate the importance of patient education in those particular areas for example:
  • Risk factors of diabetes mellitus 2 including “insulin resistance syndrome” or “metabolic syndrome”
  • Self / Home Monitoring of Blood Glucose (SMBG /HMBG)
  • Monitoring using (SMBG) and (HbA1c) for insulin dosage adjustment
  • Importance of insulin therapy in order to avoid DKA
 Diabetes mellitus concept map also includes:

Non pharmacological treatment of DM:

Modifications in diet and exercise should be adjusted individually, with different diet requirements for both types of DM.

Adjunctive treatment

Treatment and prevention of complications and recommendations of using ACEIs, ARBs, aspirin, and/or lipid-lowering agents according to patient’s case.
Diabetes Mellitus Concept Map Folded Poster
Diabetes Mellitus Folded Map

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

order diabetes mellitus concept map
Diabetes Mellitus Concept Map, version no. 2.0, by Maha Atef, B Pharm
Last updated on: 31 October 2012  

References

“American Diabetes Association Treatment Algorithm for Type 2 Diabetes.” Pharmacist’s Letter. November 2006. 11 May 2009.

“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>  // //

Parkinson Disease Concept Map

Parkinson Disease Concept Map Parkinson Disease
Parkinson Disease Concept Map
Order the full map

What is Parkinson Disease (PD)?

The map starts with disease’s definition, epidemiology, etiology, and signs and symptoms.
Parkinson disease is an idiopathic, slowly progressive, degenerative disorder that is characterized by resting tremor, stiffness (rigidity), slow and decreased movement (bradykinesia), and gait and/or postural instability. The etiology of Idiopathic Parkinson Disease (IPD) is unknown, but most likely IPD is a result of interactions between ageing, genetic predisposition, and environmental factors.
Part of Parkinson Disease (PD) Concept Map - definition, epidemiology, etiology, and signs and symptoms
Part of Parkinson Disease (PD) Concept Map – definition, epidemiology, etiology, and signs and symptoms
Common motor signs of Parkinson disease include tremor, regidity, bradykinesia, and postural instability. Each of these sings is stated in the map with corresponding features in the form of table. For example, features of bradykinesia include:
  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

Parkinson disease must be differentiated from other conditions presenting tremors, especially “Atypical Parkinsonism”. As shown in the map, atypical parkinsonism refers to a set of symptoms typically seen in PD, but caused by other disorders.  It is caused not only by cell loss in the substantia nigra pars compacta (SNc), but also by additional degeneration of cells in the parts of the nervous system that normally contain DA receptors (striatum). Also mentioned in the map:
  • 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
Parkinson disease vs atypical parkinsonism – PD differential diagnosis Zoom-out-pharmacotherapy

Parkinson’s Pathophysiology

At this part of the map, there is an inter-link between disease’s pathophysiology and treatment. Starting from disease’s pathophysiology, the main pathological feature of PD is the death of dopaminergic neurons in
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
Part of Parkinson Disease Concept Map – Pathophysiology and Treatment of Parkinson Disease

Parkinson’s Treatment

Dopamine metabolism and Antiparkinson drugs mechanisms of actions - Zoom out - Pharmacotherapy
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-zoom-out-pharmacotherapy
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 - Zoom out - Pharmacotherapy
Levodopa motor complications table – clinical features, mechanism, and management

Surgical Management of Parkinson Disease

Surgical Management of Parkinson Disease - Zoom out - Pharmacotherapy
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 - Zoom out - Pharmacotherapy
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 posterWe hope you find Parkinson Disease (PD) Concept Map helpful.  

order parkinson disease concept mapParkinson Disease (PD) Concept Map by Maha Atef, B Pharm, PGDip (ClinPharm), PGDip (TQM).

Last updated on:  26 October 2014

Obesity Concept Map

Obesity Concept Map
Obesity Concept Map

Obesity Concept Map: An Overview

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

Definition

The map starts with the definition of Obesity “obesity is excess body fat.  It is defined as a body mass index (BMI) 30 kg/m2.” and the epidemiology.  On the left side of the map, you’ll find obesity etiology and risk factors stated and represented using a funny image that will help you memorize this part easily.

Etiology and Risk Factors

Factors that contribute to obesity include:
  • 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
Obesity Etiology and Risk Factors – part of the map

Classification

According to the etiology:
  • Primary obesity
  • Secondary obesity
According to body mass index (BMI)
Classification of obesity according to Body Mass Index (BMI)
Classification of obesity according to BMI

According to waist-to-hip ratio

(fat distribution):
  • Apple obesity
  • Pear obesity

Diagnosis and Clinical Presentation

Diagnosis of obesity is based on
1-     History; it is important to assess patient’s dietary habit, physical
activity level, whether obesity is due to one of the secondary causes or not,
and if the patient have any of obesity comorbid conditions that should be
managed besides to obesity.
2-     Physical Examination, includes:
– Body mass index (BMI) = weight / height2 (kg/m2); it is used to assess the severity of obesity; see previous table
– Body composition analysis; assesses percentage of body fat and muscle.
– Waist circumference; estimates visceral fat
– Waist-to-hip ratio; measures fat distribution; accordingly obesity is classified into: Pear obesity (gynoid obesity) and Apple obesity (Android obesity)
3-     Laboratory Test that assess secondary causes and/or comorbid condition,
examples:
– Fasting lipid profile
– Fasting plasma glucose, hemoglobin A1c, and electrolyte measurements
– Serum thyroid stimulation hormone and free T4 measurement

Complications and Comorbidities

They are stated in the map using a simple figure showing sites of organs exposed to obesity complications.  Overall they can be: psychosocial, neurological, cardiovascular, endocrinal, musculoskeletal, renal, gastrointestinal, and/ or pulmonary.
Using the previously mentioned aspects of obesity – risk factors, secondary causes and information got from
diagnosis and clinical presentation – individualized treatment goals and plan are to be set.


Treatment of Obesity

The map includes treatment goals and approach.
First line therapy for obesity is Non-Pharmacological Treatment including: Low-calorie diet (LCD), Exercise, and Behavioral Modification – benefits of each and more details are stated in the map.
Pharmacotherapy – presented in the form of comparison; comparing:
         Centrally acting anorexiant medications (impair dietary intake)
First, Agents Approved for Long-Term Use (Lorcaserin – Phentermine/Topiramate ER)
Second, Agents Approved for Short-Term Use (Phentermine – Diethylpropion)
         Peripherally acting medications (impair dietary absorption): Orlistat
Bariatric Surgery – the map explains its indications, benefits, most common procedures (Adjustable gastric banding –
Roux-en-Y gastric bypass (RYGB)), and post-operative maintenance and supplementation.
This map will help you link between obesity etiology and/or risk factors and diagnosis for the aim of individualizing therapy.
Obesity Concept Map Folded Poster
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.

order obesity concept map
Obesity concept map is written by:
Hagar M. Abdel AA’l, B Pharm.

Reviewed and edited by Maha Atef, B Pharm.

Last updated on: 7 February 2013