Varicella-zoster virus (VZV) is a linear, double-stranded DNA virus in the Herpesviridae family. Varicella-zoster infections are highly contagious and transmitted through aerosolized

respiratory droplets or contact with infected skin lesions. Chickenpox is the primary infection and occurs most commonly in children.

GENERAL CHARACTERISTICS & EPIDEMIOLOGY:

Basic features of varicella-zoster virus (VZV) (human herpesvirus 3).

• Taxonomy:

1. Family: Herpesviridae

2. Subfamily: Alphaherpesvirinae

3. Genus: Varicellovirus

4. DNA virus:

5. Linear

6. Double stranded

7. Structural elements:

8. Core (genetic material)

9. Icosahedral protein capsid

10. Tegument (viral proteins and enzymes)

11. Lipid envelope and glycoprotein spikes

• Associated diseases

Varicella-zoster virus causes 2 distinct syndromes:

1. Chickenpox

2. Shingles (herpes zoster)

Epidemiology

• Chickenpox:

Prior to routine vaccine use:

• > 95% of people infected by the age of 20 years

• Annual incidence in the United States: 4 million cases

• Approximately 11,000 hospital admissions

• Approximately 100 deaths

Since the vaccine:

• Decrease in incidence by 90%

• Substantial decrease in hospitalization and deaths

Shingles:

• Annual incidence in the United States: 1.2 million cases

• Approximately 30% of the population will experience herpes zoster during their lifetime.

• Occurs only in individuals previously affected with chickenpox

PATHOGENESIS

Reservoir: Humans are the only reservoir for VZV.

Transmission: Infections are highly contagious and the virus may be transmitted through:

• Inhalation of aerosolized respiratory droplets

• Direct contact with the vesicle fluid from skin lesions

Host risk factors: Individuals at higher risk for severe disease and complications:

• Pregnant women

• Age extremes: Infants & lderly

• Immunocompromised patients: HIV/AIDS, organ transplantation, chemotheray, chronic steroids.y

CLINICAL PRESENTATION

Chickenpox:

Chickenpox is caused by a primary infection with VZV and has an incubation period of 10‒ 21 days after exposure.

• Prodrome (more common in adolescents and adults):

Fever

Malaise

Pharyngitis

Loss of appetite

Headache

• Enanthem:

May precede exanthem

Small shallow ulcers

Can be pruritic or painful

• Exanthem:

Intensely pruritic

• Evolution:

Small macules → papules → vesicles on red base (“dew drop on a rose petal”)

Become pustular → crusted

Appear in crops over the course of a few days → lesions will be in different

stages of evolution

• Distribution:

Generalized: May include the palms and soles

DIAGNOSIS & MANAGEMENT

Diagnosis:

The diagnosis of chickenpox is most often clinical. The following tests may be used to

diagnose patients with atypical presentations:

• PCR

• Most sensitive method: Direct fluorescent antibody (DFA) test.

• Serology

• Tzanck smear

MANAGEMENT

Supportive care:

• Pruritus management:

1. Oatmeal baths

2. Calamine lotion

3. Antihistamines

4. Antipyretics:

5. Acetaminophen

6. Avoid aspirin in children.

   
   

   Avoid scratching skin lesions to prevent: Secondary bacterial infections & permanent scarring

• Antiviral therapy:

1. Recommended for patients at risk for severe complications:

2. Unvaccinated adolescents

3. Children on chronic salicylate therapy

4. Unvaccinated or vaccinated adults

5. Pregnant women

6. Immunocompromised patients

Options:

• Acyclovir

• Valacyclovir

• Famciclovir

• Administer within 24 hours of rash onset.

PREVENTION

Live attenuated vaccine:

↓ Risk of disease by 80% and risk of severe disease by > 99%

• 2-dose schedule for children:

1. Start at 12‒15 months of age

2. Booster at 4‒6 years of age

• Contraindications:

Immunocompromised patients

Pregnant women

Parkinson's disease (PD) is a chronic, progressive neurodegenerative disorder. Although the cause is unknown, several genetic and environmental risk factors are currently being studied.

Individuals present clinically with resting tremor, bradykinesia, rigidity, and postural instability.

EPIDEMIOGY

One of the most common neurodegenerative disorders

• Annual incidence: 4.5–21 cases per 100,000 population

• Mean age at onset: approximately 60 years

• Lifetime risk: approximately 2% for men and 1.3% for women

ETIOLOGY

The etiology of PD is unclear but depends on various genetic and environmental factors.

• Risk factors

Environmental and nongenetic risk factors:

1. Exposure to pesticides

2. Exposure to nitrogen dioxide

3. History of traumatic brain injury

4. Exposure to hydrocarbon solvents

5. Living in a rural environment

6. Living in proximity to industrial plants or quarries

7. Drinking well water

8. Use of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown to cause irreversible parkinsonism.

9. Excess body weight

10. Type 2 diabetes

11. Gene mutations associated with PD

CLINICAL PRESENTATION

The signs of PD are progressive and gradually appear over a long period of years to decades.

• Cardinal motor manifestations:

1. Bradykinesia = slowness of movements

2. Decreased manual dexterity of the fingers

3. Difficulty in completing simple tasks such as tying shoelaces, buttoning clothes, and

4. picking up small objects.

5. Short shuffling gait

6. Loss of coordination of movements as the disease progresses

   • Advanced stages: Freezing of movements may occur.

7. Tremor: Resting tremor described as a “pill-rolling” tremor

8. That can involve the hands, legs, lips, jaw, and tongue.

9. Rigidity

10. Cogwheel rigidity = a pattern of resistance and relaxation in passive movement

11. “Lead pipe” rigidity may also be seen in a few individuals = tonic resistance that is smooth in passive movement

12. Rigidity affecting the face: characteristic “masked” expression

13. Postural instability = impairment of postural reflexes resulting in a feeling of imbalance and

14. a tendency to fall

• Other motor manifestations

1. Speech impairment

2. Laryngeal dysfunction and dysphagia

3. Blurred vision

4. Micrographia

5. Stooped posture

6. Myoclonus

• Gait abnormalities

• Nonmotor symptoms:

Autonomic dysfunction presenting as:

1. Orthostasis

2. Constipation

3. Diaphoresis

4. Urinary difficulties

5. Sexual dysfunction

• Olfactory dysfunction: anosmia

• Mood disorders, including depression and anxiety

• Pain and sensory disturbances

• Cognitive dysfunction and dementia

• Psychosis

• Hallucinations

Sleep disturbances:

1. Insomnia

2. Daytime sleepiness

3. REM sleep behavior disorder (RBD)

DIAGNOSIS

The diagnosis of PD is made by clinical history and neurologic examination.

Diagnosis requires 4 things:

1. Motor parkinsonism

2. No absolute exclusion criteria

3. At least 2 supportive criteria

4. No red flags

Motor parkinsonism, an essential criterion of PD, requires bradykinesia and at least 1 of the following:

• Resting tremor

• Rigidity

• Postural instability

TREATMENT & MANAGEMENT

Management:

The goal of management is to treat the symptomatic motor and nonmotor features of the disorder to improve quality of life.

Treatment

General measures:

• Physical therapy

• Occupational therapy

• Emotional support

Medical therapy:

1. Levodopa

2. MAO-B inhibitors.

3. Non-Ergot dopamine antagonists

PREVALENCE

The prevalence of diagnosed diabetes is 12.6% and undiagnosed diabetes is 5.8%1

Type 2 diabetes is more common in older adults due to factors such as age, lifestyle, and genetics

SYMPTOMS

• Bladder, kidney, skin, or other infections that are more common or heal slowly

• Fatigue

• Hunger

• Increased thirst

• Increased urination

• Blurred vision

CAUSES

Insulin is a hormone produced by the pancreas, which helps move glucose from the blood to the body's cells for storage, but when the patient has type 2 diabetes the cells of their body do not react well to insulin making a resistance to it that causes glucose not to enter the cell to be stored and we have elevated blood glucose

DIAGNOSIS

• fasting blood glucose level

• hemoglobin AC1 test

• oral glucose tolerance test

TREATMENT

Treatment of type 2 diabetes involves lifestyle changes, such as diet and exercise, along with oral medications or insulin injections as needed.

PREVENTION

To prevent type 2 diabetes, it's important to maintain a healthy lifestyle. This includes maintaining a proper weight through a balanced diet and regular exercise. In addition, it is crucial to control blood sugar, avoid tobacco, and limit alcohol consumption. Reducing stress and getting regular medical checkups are also important.

IMPACT IN LIFE

Type 2 diabetes can impact a person's life in a number of ways. It requires lifestyle changes, such as diet and exercise, and can increase the risk of serious health problems. It can also affect mental health, personal relationships, and have a financial impact due to the costs associated with treatment.

CAUSES AND SYMPTOMS

Cytomegalovirus (CMV) is a common virus. Once infected, your body retains the virus for life. Most people don't know they have cytomegalovirus (CMV) because it rarely causes problems in healthy people.

If you're pregnant or if your immune system is weakened, CMV is cause for concern. Women who develop an active CMV infection during pregnancy can pass the virus to their babies, who might then experience symptoms. For people who have weakened immune systems, especially people who have had an organ, stem cell or bone marrow transplant, CMV infection can be fatal.

CMV spreads from person to person through body fluids, such as blood, saliva, urine, semen and breast milk. There is no cure, but there are medications that can help treat the symptoms.

RISK FACTORS

Over half of adults have been infected with CMV by age 40, most with no signs or symptoms. CMV is transmitted by direct contact with infectious body fluids, such as urine, saliva, blood, tears, semen, and breast milk. CMV can be transmitted sexually and through transplanted organs and blood transfusions.

PEOPLE IN RISK

For people who have weakened immune systems, CMV infection can be serious or even fatal. People who have undergone stem cell or organ transplants seem to be at greatest risk.

TREATMENT

A provider can treat CMV with the antiviral medications ganciclovir (GCV) or valganciclovir (VGC). These drugs are given directly into your vein (IV infusion) or swallowed in a pill. Providers usually only treat CMV in people who have a compromised immune system or babies who are born with symptoms of CMV.

HOW TO PREVENT

Careful hygiene is the best prevention against CMV . You can take these precautions: Wash your hands often. Use soap and water for 15 to 20 seconds, especially if you have contact with young children or their diapers, saliva or other oral secretions.

IMPACT IN LIFE

Occasionally, CMV can cause mononucleosis or hepatitis (liver problem). People with weakened immune systems who get CMV can have more serious symptoms affecting the eyes, lungs, liver, esophagus, stomach, and intestines. Babies born with CMV can have brain, liver, spleen, lung, and growth problems.

REFERENCES

• About Cytomegalovirus and congenital CMV infection. (2023, marzo 6). Cdc.gov. https://www.cdc.gov/cmv/overview.html

• Cytomegalovirus (CMV) infection. (2022, marzo 23). Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/cmv/symptoms-causes/syc-20355358

• Cytomegalovirus (CMV). (s/f). Cleveland Clinic. Recuperado el 8 de marzo de 2024, de https://my.clevelandclinic.org/health/diseases/21166-cytomegalovirus

  
  

  
  
  

CAUSES

It is caused by the measles virus, which belongs to the paramyxovirus family.

SYMPTOMS

Symptoms of measles usually begin 10–14 days after exposure to the virus. A prominent rash is the most visible symptom.

Early symptoms usually last 4–7 days. They include:

• running nose

• cough

• red and watery eyes

• small white spots inside the cheeks.

The rash begins about 7–18 days after exposure, usually on the face and upper neck. It spreads over about 3 days, eventually to the hands and feet. It usually lasts 5–6 days before fading.

DIAGNOSIS

The doctor can diagnose measles from the characteristic rash of the disease and also by small bluish-white dots with a deep red background on the inside of the cheek.

TREATMENT

There is no specific treatment for measles. Caregiving should focus on relieving symptoms, making the person comfortable and preventing complications.

Doctors may use antibiotics to treat pneumonia and ear and eye infections.

PREVENTION

Administer the measles vaccine

PREVELENCE

Prevalence has decreased thanks to vaccination, but remains more common in children due to their partial immunity, social interaction in settings such as daycare centers and schools, and lack of vaccination in some cases.

INPACT IN LIFE

Measles can have a serious impact on children's health and well-being, causing severe symptoms and complications such as pneumonia and encephalitis. The disease can result in missed school, emotional stress for the child and family, and possible long-term complications

CAUSES

Infarction is tissue death (necrosis) due to inadequate blood supply to the affected area. It may be caused by artery blockages, rupture, mechanical compression, or vasoconstriction. The resulting lesion is referred to as an infarct (from the Latin infarctus, "stuffed into").

SYMPTOMS

The symptoms of MI include chest pain, which travels from left arm to neck, shortness of breath, sweating, nausea, vomiting, abnormal heart beating, anxiety, fatigue, weakness, stress, depression, and other factors.

RISK FACTORS

• Move

• Speak

• Eat

• Think and remember

• Control your bowel and bladder

• Control your emotions

• Control other vital body functions

PEOPLE IN RISK

Lifestyle risk factors include:

• Being overweight or obese

• Physical inactivity

• Heavy or binge drinking

• Use of illegal drugs, such as cocaine and methamphetamine

Medical risk factors include:

• High blood pressure

• Cigarette smoking or secondhand smoke exposure

• High cholesterol

• Diabetes

• Obstructive sleep apnea

• Cardiovascular disease, including abnormal rhythm, such as atrial fibrillation

• Hormone use, such as the use of birth control pills or hormone therapies that include estrogen

Other factors that you can't control are associated with a higher stroke risk, including:

• Age
  People 55 or older have a higher risk of stroke than younger people.

• Race
  African American and Hispanic patients have a higher risk of stroke than people of other races.

• Sex
  Men have a higher risk of stroke than women. Women are usually older when they have strokes, and they're more likely to die of strokes than men. It kills more than twice as many U.S. women as breast cancer each year.

TREATMENT

An IV injection of recombinant tissue plasminogen activator (TPA) is the gold standard treatment for ischemic stroke. The two types of TPA are alteplase (Activase) and tenecteplase (TNKase). An injection of TPA is usually given through a vein in the arm within the first three hours.

HOW TO PREVENT

Many strokes could be prevented through healthy lifestyle changes and working with your health care team to control health conditions that raise your risk for stroke.

IMPACT IN LIFE

A stroke can change your thinking and memory, and also how you see, hear and feel the world. This can affect how you feel about yourself, your family and friends. Thinking and memory skills are also known as cognitive skills.

REFERENCES

• CDC. (2023, septiembre 25). Prevent stroke: What you can do. Centers for Disease Control and Prevention. https://www.cdc.gov/stroke/prevention.htm

• Micah Yost, D. O. (2021, mayo 17). Who is most at risk for a stroke? Mayo Clinic Health System. https://www.mayoclinichealthsystem.org/hometown-health/speaking-of-health/who-is-most-at-risk-for-a-stroke

• Stroke. (s/f). Hopkinsmedicine.org. Recuperado el 8 de marzo de 2024, de https://www.hopkinsmedicine.org/health/conditions-and-diseases/stroke

  
  

  
  

Alzheimer disease is a progressive neurodegenerative disease that causes brain atrophy. and a decline in cognition, memory, and social skills.

Epidemiology

• Leading cause of dementia in adults > 65 years

• Incidence: women > men

• Incidence increases exponentially after age 65.

• Prevalence of Alzheimer disease after age 70 in the United States: 9.7%

• Familial Alzheimer disease called "early-onset" Alzheimer disease:

• Rare (< 1% of cases)

• Caused by genetic mutations

• Autosomal dominant

Etiology

Although the cause of Alzheimer disease is unknown, several genetic defects and risk factors have been identified.

Clinical Presentation

Interviewing family members is essential to obtain a history of cognitive and behavioral changes.

Memory impairment

Memory impairment is the most common early symptom of Alzheimer disease.

• Described as anterograde long-term episodic amnesia

• Insidious onset with slow gradual progression

• In earlier stages of presentation: episodic memory is affected = memory of events occurring at a time and place

• In later stages of memory impairment:

• Procedural learning and remote memory.

• Semantic memory = memory for facts, vocabulary, and concepts

• Immediate recall

Impaired executive function and judgment

• Subtle to prominent impairment occurs in early Alzheimer disease.

• Ability to complete tasks declines

• Reduced insight into deficits (anosognosia) 1 over time

• Associated with behavioral changes

Impairment in cognitive domains

• Develop and progress insidiously

• Visuospatial impairments: seen relatively early in the disease

• Language deficits and primary progressive aphasia: manifest later

Motor function impairment

• Apraxia = difficulty performing purposeful movements

• Usually occurs after deficits in memory and language are apparent

• Initially presents with difficulty performing complex, multistep activities

• Later - difficulty with dressing, using utensils, and other self-care tasks

• Shuffling gait with generalized muscle rigidity

• Slowness and awkwardness of movement

Behavioral and psychological symptoms

• Sleep disturbances

• Apathy/social disengagement

• Irritability

• Agitation, aggression, wandering, and psychosis: difficult for family members

• Delusions in later stages: common themes of theft, infidelity, or misidentification

References

1. Seeley, W. W., Miller, B. L. (2018). Alzheimer's disease. In: Jameson, J.L., et al. (Eds.), Harrison's Principles of Internal Medicine, 20th ed., vol. 2. McGraw-Hill, pp. 3108-3114

2. Wolk, D. A., Dickerson, B. C. (2020). Clinical features and diagnosis of Alzheimer disease. UploDate. Retrieved August 3, 2021, from https://www.uptodate.com/contents/clinical-features-and-diagnosis-of-alzheimer-disease

3. Keene, C. D., Montine, T. J., Kuller, L. H. (2018). Epidemiology, pathology, and pathogenesis of Alzheimer disease. UpToDate. Retrieved August 3, 2021, from https://www.uptodate.com/contents/epidemiology-pathology-and-pathogenesis-of-alzheimer-disease

4. Lakhan, S. E. (2021). Alzheimer Disease. Medscape. Retrieved August 3, 2021, from https://emedicine.medscape.com/article/1134817

5. Kumar, A., et al. Alzheimer disease. StatPearls. Retrieved August 3, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK499922/

6. Maccioni, R.B., González, A., Andrade, V., Cortés, N., Tapia, J.P., Guzmán-Martínez, L. (2018). Alzheimer's disease in the perspective of neuroimmunology. Open Neurol J 12:50-56.
   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6040210/

7. Atri, A. (2019). The Alzheimer's Disease Clinical Spectrum: Diagnosis and Management. Medical Clinics of North America, vol. 103, no. 2. Elsevier, pp. 263-293. https://doi.org/10.1016/j.mcna.2018.10.009

8. Alzheimer's Association. (2021). Alzheimer's disease facts and figures.
   https://www.alz.org/media/Documents/alzheimers-facts-and-figures.pdf

CAUSES

The cause depends on the type of arthritis. Osteoarthritis is caused by the wear and tear of the joint over time or because of overuse. Rheumatoid arthritis, lupus, and scleroderma are caused by the body's immune system attacking the body's own tissues. Gout is caused by the buildup of crystals in the joints.

SYMPTOMS

Common symptoms of arthritis include pain, redness, heat, and swelling in your joints. If you have arthritis, it is important for your doctor to diagnose the type of arthritis you have so that you can get the proper treatment.

RISK FACTORS

• Overweight and Obesity: Excess weight can contribute to both the onset and progression of knee and hip osteoarthritis.

• Physical inactivity: Is associated with increased severity and progression of many types of arthritis.

• Joint Injuries: Damage to a joint can contribute to the development of osteoarthritis in that joint.

• Smoking: Is linked to the progression and severity of rheumatoid arthritis and systemic lupus erythematosus.

• Infection: Many microbial agents can infect joints and potentially cause the development of various forms of arthritis.

• Occupation: Certain occupations involving repetitive knee bending and squatting are associated with osteoarthritis of the knee and hip.

• Diet: Plays an important role in healthy weight maintenance, which is a key factor in the prevention/reduction of disease progression. It is also an identified risk factor for the development and management of gout.

PEOPLE IN RISK

People born with specific genes are more likely to develop certain types of arthritis, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and ankylosing spondylitis. These genes are called HLA (human leukocyte antigen) class II genotypes. These genes can also make your arthritis worse.

DIAGNOSE

Your healthcare provider will take your medical history and give you a physical exam. Tests may also be done. These include blood tests such as:

• Antinuclear antibody (ANA) test. This checks antibody levels in the blood.

• Complete blood count (CBC). This checks if your white blood cell, red blood cell, and platelet levels are normal.

• Creatinine. This test checks for kidney disease.

• Sedimentation rate. This test can find inflammation.

• Hematocrit. This test measures the number of red blood cells.

• RF (rheumatoid factor) and CCP (cyclic citrullinated peptide) antibody tests. These can help diagnose rheumatoid arthritis. They can also assess how severe the disease is.

• White blood cell count. This checks the level of white blood cells in your blood.

• Uric acid. This helps diagnose gout.

Other tests may be done, such as:

• Joint aspiration (arthrocentesis). A small sample of synovial fluid is taken from a joint. It's tested to see if crystals, bacteria, or viruses are present.

• X-rays or other imaging tests. These can tell how damaged a joint is.

• Urine test. This checks for protein and different kinds of blood cells.

• HLA tissue typing. This looks for genetic markers of ankylosing spondylitis.

• Skin biopsy. Tiny tissue samples are removed and checked under a microscope. This test helps to diagnose a type of arthritis that involves the skin, such as lupus or psoriatic arthritis.

• Muscle biopsy. Tiny tissue samples are removed and checked under a microscope. This test helps to diagnose conditions that affect muscles.

TREATMENT

• Medications. Short-term relief for pain and inflammation may include pain relievers such as acetaminophen, aspirin, ibuprofen, or other nonsteroidal anti-inflammatory medications.

• Heat and cold. Pain may be eased by using moist heat (warm bath or shower) or dry heat (heating pad) on the joint. Pain and swelling may be eased with cold (ice pack wrapped in a towel) on the joint.

• Joint immobilization. The use of a splint or brace can help a joint rest and protect it from further injury.

• Massage. The light massage of painful muscles may increase blood flow and bring warmth to the muscle.

• Transcutaneous electrical nerve stimulation (TENS). Pain may be reduced with the use of a TENS device. The device sends mild, electrical pulses to nerve endings in the painful area. This blocks pain signals to the brain and changes pain perception.

• Acupuncture. This is the use of thin needles that are inserted at specific points in the body. It may stimulate the release of natural, pain-relieving chemicals made by the nervous system. The procedure is done by a licensed health care provider.

HOW TO PREVENT

The fact is, there is no sure way to prevent arthritis. But you can help reduce your risk and delay the potential onset of certain types of arthritis. If you have healthy joints right now, do all you can now to maintain mobility and function and avoid the pain and disability associated with arthritis.

There are more than 100 types of arthritis and related conditions, and each has associated risk factors, individual features, behaviors and circumstances.

Some risk factors are not modifiable, and there really isn’t anything you you can do about them. Being female and having a family history of arthritis (genetic profile) are two examples of factors that make people more likely — but not certain — to get some types of arthritis.

Risk factors that are considered modifiable are the behaviors and circumstances that can be changed in order to reduce risk, delay onset or even prevent arthritis. A few examples of modifiable risk factors for certain types of arthritis and related conditions:

• Osteoarthritis: Maintain a healthy weight.

• Rheumatoid arthritis: Do not smoke.

• Gout: Eat a healthful diet that’s low in sugar, alcohol and purines.

IMPACT IN LIFE

Rheumatoid arthritis causes joint pain and swelling, reduced mobility and physical weakness. General tiredness, trouble sleeping and exhaustion are other common symptoms. All of these symptoms can greatly affect your everyday life and overall wellbeing. Living with rheumatoid arthritis isn't always easy.

REFERENCES

• Everyday life with rheumatoid arthritis. (2020). Institute for Quality and Efficiency in Health Care (IQWiG).

• NIAMS. (2017, abril 14). Arthritis. National Institute of Arthritis and Musculoskeletal and Skin Diseases. https://www.niams.nih.gov/health-topics/arthritis

  
  Arthritis. (s/f). Hopkinsmedicine.org. Recuperado el 8 de marzo de 2024, de https://www.hopkinsmedicine.org/health/conditions-and-diseases/arthritis

  
  
  

Brutsaert, E. F. (2024, 21 febrero). Diabetes mellitus (DM). MSD Manual Professional Edition. https://www.msdmanuals.com/professional/endocrine-and-metabolic-disorders/diabetes-mellitus-and-disorders-of-carbohydrate-metabolism/diabetes-mellitus-dm

Oiseth, S., Jones, L., & Maza Guia, E. (2024, 4 marzo). Parkinson Disease (Clinical). Lecturio. https://www.lecturio.com/concepts/parkinson-disease-clinical/

Oiseth, S., Jones, L., & Maza Guia, E. (2022, 8 septiembre). Varicella-Zoster Virus/Chickenpox. Lecturio. https://www.lecturio.com/concepts/varicella-zoster-virus-chickenpox/

EPIDEMIOLOGY & ETIOLOGY

Type 1 accounts for < 10% of all cases of diabetes mellitus.

In type 1 diabetes mellitus (previously called juvenile-onset or insulin-dependent), insulin production is absent because of autoimmune pancreatic beta-cell destruction possibly triggered by an environmental exposure in people who are genetically susceptible. Type 1 diabetes generally develops in childhood or adolescence and until recently was the most common form diagnosed before age 30; however, it can also develop in adultos.

Some causes are autoimmunity problems, diet, generic predisposure & viruses.

SIGNS & SYMPTOMS

The most common symptoms of diabetes mellitus are those of hyperglycemia. The mild hyperglycemia of early diabetes is often asymptomatic; therefore, diagnosis may be delayed for many years if routine screening is not done.

Patients with type 1 diabetes typically present with symptomatic hyperglycemia and sometimes with diabetic ketoacidosis (DKA). However, they develop diabetes-related autoantibodies and dysglycemia before becoming symptomatic.

DIAGNOSIS

• Fasting plasma glucose (FPG) levels

• Glycosylated hemoglobin (HbA1C)

• Sometimes oral glucose tolerance testing

TREATMENT & MANAGEMENT

1. Diet and exercise

2. For type 1 diabetes, insulin

3. To prevent complications, often renin-angiotensin-aldosterone system blockers (angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers), and statins.

The goal of diabetes treatment is control of hyperglycemia to relieve symptoms and prevent complications while minimizing hypoglycemic episodes. Diabetes mellitus control can be monitored by measuring blood levels of

1. Glucose

2. HbA1C

3. Fructosamine