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Upper respiratory disease
EPIDEMIOLOGY OF RESPIRATORY DISEASE IN CHILE AND THE WORLD
Mortality
3rd cause of death in Chile (after cardiovascular and cancer)
Rising mortality
1991: 61/100.000: 10% total deaths
1999: 76/100.000: 14%
For specific pathology
For pneumonia: the elderly
For asthma and COPD: stationary
High Respiratory Diseases
IRA - was
conceptually be categorized as acute respiratory diseases
Virus principal agents
Many respiratory diseases are interpreted and episodic
The carina is the lower limit high-low
Determines strong burden of care, economic and social
RHINITIS:
Rhinorrhea
Itching
Nasal obstruction (blocking)
Sneezing
SINUSITIS:
Localized pain
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Rhinosinusitis
Acute Respiratory Disease: Classification
Infectious
Allergic
Non Infectious - nonallergic
ALLERGIC rhinosinusitis
Seasonal: aeroallergen pollen, fungal spores.
Perennial aeroallergens, hypersensitivity ASA, beta blockers
Occupational: latex, flour, sawdust, ATB, enzymatic detergents, etc..
Food: Assoc. urticaria and asthma. Milk, eggs, fish, wheat, peanut, soybean and response to histamine (cheese, wine).
Infectious rhinosinusitis
Acute common cold (> 90%), bacterial sinusitis (Haemophilus influenzae, STP pneumoniae (50%)
Chronic Bacterial anatomical errors, Panhypogammaglobulinemia congenital Human Immunodeficiency Virus, primary ciliary dysfunction.
No infectious rhinitis - No allergic
IDIOPATHIC: Vasomotor
HORMONES: Pregnancy, estrogens
DRUGS: Hypersensitivity ASA, NSAIDs and vessel constrictor.
ERA Treatment
Allergic rhinitis ® Identify and avoid allergens, antihistamines, topical corticosteroids
Vasomotor rhinitis ® Topical anticholinergics
Acute sinusitis ® analgesics, hydration, vasopressors ATB
Acute pharyngitis
Pain in the pharyngeal region, which is accentuated in swallowing. sometimes there are irritative cough, redness is seen pharyngeal area.
Etiology
Beta-hemolytic streptococcus alone accounts for 10% of cases, the vast majority are self-limited, viral and require only general measures
Acute pharyngitis
Suspected streptococcal if it meets at least three of the following clinical criteria: fever, amigdaliano exudate, tender cervical lymphadenopathy, absence of cough
Common Respiratory Viruses
Viral respiratory diseases are the most common diseases is estimated that up to 75% of acute respiratory illnesses are viral etiology.
The impact is significant:
30 to 50% of work time lost
60 to 80% of school absenteeism
Frequency Associated With Respiratory Syndrome Virus

PLEURAL EFFUSION
Accumulation of> 20 cc of fluid in the pleural
By increasing production
By decreased reabsorption
1 is a manifestation of disease
Can express the complication of diseases

IS PRESENTED IN 10% OF ENF. SYSTEMIC
40% IS FOR HEART FAILURE
60% FOR OTHER DISEASES

Cardiogenic pleural effusions
48% parapneumonic
75% of bacteria.
25% viral
24% neoplastic
50% lung or breast
tep 18%
cirrhosis
Morphology and Physiology Anatomy Pleural
Pleural cavity: closed space bounded by the pleura, which has negative pressure
Pleura: serosa with two leaves
Visceral: covering the lung surface including the interlobar fissures.
Parietal: covers the surface of the chest wall, mediastinum and diaphragm.
Visceral pleura
Human visceral pleura is thick, and its blood supply comes Delas art. bronchial
The visceral pleura does not give pain
Venous drainage goes to the azygos system
Parietal pleura
If I have a tumor at the level of nodes intercostal be fluid buildup.
Lymphatic drainage channels are lockable
Nerve vascular bundle runs along the bottom edge of the rib.
Order: vessels, arteries and nerves from the top down
There stomata of the parietal pleura
The pl. parietal innervation is rich, painful
Microscopic structure of the pleura
5 layers for light microscopy:
Mesothelial cell layer
Connective tissue submesothelial
Fibroelastic superficial layer.
Loose connective tissue
(fat cells, vessels sang. and lymphatic)
Fibro-elastic layer deep.
ULTRASTRUCTURE of mesothelial cells
Fine structure of mesothelial cells:
Microvilli.
Pinocytotic vesicles.
Tight junctions and desmosomes at the apical pole.

Role of the mesothelium
Send ac cavities. hyaluronic, which is sticky, so there is less friction
There is a greater concentration in the base than at apex and in the visceral pleura on the parietal.
TRANSPORT THROUGH AND LAPLEURA mesothelial cells
Physical
Communications pleurolinfáticas
Physical transport
Molecules <4 nm pass freely.
Larger molecules are generating different types of vesicles within the mesothelial cell.
Molecules larger than 1000 nm do not penetrate the basement membrane.

COMMUNICATIONS PLEUROLINFÁTICAS
- Stomata.
Cribriform-membrane.
"Gaps and lymphatic channels.
PLEURAL FLUID CHARACTERISTICS
Volume: 0.1 to 0.2 mL / kg body weight (15 cc)
Light color
Odor: odorless
Protein concentration + / - 1 and 1.5 g / dL.
pH is alkaline: pH 7.66
[chlorine and sodium] are slightly lower than in plasma
[Baking]: 20 to 25% compared to the plasma
Potassium: equal to plasma
Glucose: 144 nearly equal to plasma
LDH: 129 is <half the value of serum
PHYSIOLOGICAL CHARACTERISTICS OF PLEURAL FLUID
Cells: 1500 cells / ml
monocytes (30-75%)
mesothelial cells (70%)
lymphocytes (2-30%)
neutrophils (10%)
(no red blood cells)
DYNAMIC BALANCE
Depends on:
The game of hydrostatic and colloid osmotic pressure between the visceral and parietal capillaries
The integrity of the serous
Lymphatic drainage
FACTORS THAT DETERMINE THE BALANCE
THE VARIOUS COMPARTMENTS
Magazines
systemic capillary, interstitium parietal, parietal pleura, pleural space, visceral pleura, interstitial lung, pulmonary capillary.
Subatmospheric pressure of the tissues surrounding the pleura.
Starling's Law
Clearance of fluid in the interstitium
FLUID CLEARENCE in the interstitium
Filtration of fluid through the pleura
Drainage of fluid through the pleura
- Starling equation
The fluid flow occurs from systemic microvasculature into the interstitium extrapleural from here
into the pleural space because there is a small pressure gradient.
- It generates a flow of 0.1 to 0.02 ml / kg / h
DRAINING OF FLUIDS THROUGH PLEURA
The absorption of fluids in the visceral pleura is negligible 75% of the drainage of fluid from the pleural space occurs because the lymphatic capillaries of the parietal pleura. The lymphatics of the pleura are subadmosfericas pressure (-10 cm H2O).
GRADIENT THAT PUSHES THE FLUIDS
Is given by 3 mechanisms:
Throbbing 1.Naturaleza the lymphatics
2.Contracción smooth muscle that surrounds
3.Oscilaciones pressure during breathing movements.
This determines 60% of the flow of fluids.
The other 40% is determined by the pressure gradient from the systemic to the pulmonary microvasculature.
EMBRYOLOGY
The pericardial cavity, pleural and peritoneal come from a common origin: the coelomic cavity
Normally there are nodes connecting the pleural cavity with peritoneal
Throughout life may have defects in the serous and even of small size, can promote pathology

Semiology of the pleural effusion

Image

Causes of pleural effusion
1 .- increased hydrostatic pressure
Starling: the mov liq depends on my p º hydrostatic capillary (GC)
If I am in heart failure, will force fluid out of the capillary into the alveoli
2 .- Increased capillary membrane permeability
For inflammatory processes:
50% pneumonia will spill
3 .- Decreased oncotic pressure
Cirrhosis
Sd. nephrotic
Malnutrition
4 .- Atelectasis producing> p º (-)
5 .- Reduced lymphatic drainage
6 .- abdomen communications
from ascites of cirrhotic
For inflammation of pancreatitis
Of a hemoperitoneum with blood
RADIOLOGY OF SPILL
Chest radiograph PA-L-lateral decubitus
Uni or bilateral
Minimal or mass
Curve Damasseaux
Infrapulmonar
Cystic
STUDY PLAN FOR SPILL
Certify the diagnosis
Anamnesis:
pleuritic pain for swelling
Decompensation of an ICC
Physical Ex
Dullness water (tactile perception)
Poor inspection
Auscultation: breath pleuritic (more is heard in expiration)
Diminished vocal vibrations
Consider risk factors.
History.
Imaging study and procedures
Radiography
Pleural tap
Pleural biopsy (needle or VTC)
Ecotomografía
FBC
VTC
Surgery
CONFRONTATION DIAGNOSIS

Image


PLEURAL FLUID STUDIES
Pleural tap
Liquid extraction study
Decompression of the pleural
Gross appearance
Physical chemical study (glucose, protein, LDH, cellular)
Gram stain, aerobic culture, anaerobic and koch
Pleural fluid ADA
PH and pleural fluid cytology
Transudate
Its causes are not in the pleura
Most will be by ICC
I make, without putting drainage
Measure the liquid elements
Protein
LDH
ADA
View all breakpoints and relationships
Protein: <3 g/00 (30 g/000)
LDH: 80 mg / dl
Pleural protein / prot pl:> 0.5
Pleural LDH / LDH plasm> 0.6
pH, low ADA <40


Exudate VALUES
Proteins pleural / plasma> 0.5
Protein> 3 g/00
LDH pleural / plasma> 0.6
Pleural LDH / normal plasma value> 2 / 3
Cytology: 51% is dominated MN
RELEASE CHARACTERISTICS
Spills mononuclear predominance by:
Mononuclear: chronic inflammation: ex. Pleural TB - cancer
PMNN mean that the inflammation is acute, for example. pneumonia (7 days)
Effusions with low pH
pH <7.0 esophageal rupture
pH> 7.0 to 7.20 empyemas
STUDY SUMMARY
Physiology pleural
Need for accurate diagnosis
Pleural tap
Differentiate between transudate and exudate
Define cytology if acute or chronic
Biopsy only the exudates
PLEURAL OCCUPANCY RATES
PLEURAL EFFUSION
Hydrostatic
Infectious
Inflammatory
Neoplastic
SOLID (tumors)
CYSTS (hydatidosis)
AIR (pneumothorax)
Blood (hemothorax)
Viscera (ruptured diaphragm)
OCCUPATION BY PLEURAL FLUID
Spill-free, lower location, superior Concavity
History of coughing, pain, purulent sputum and fever.
PLEURAL OCCUPATION BY BLOOD
Posterior inferior pleural effusion
History of penetrating trauma, pleuritic pain and dyspnea.
DG: Hemothorax
Hemothorax
Collection of blood in the pleural cavity.
Pleurocrito bloody fluid with> 15% (at least> 50% Hct. Blood)
Etiology:
Chest injury (more common), pulmonary Ca, Ca pleural
Coagulation defects, thoracic surgery, cardiac surgery,
Pulmonary infarction
Pleural effusion with pus
Young patient with high fever
Recent pneumonia treated badly
Pleuritic
Redness of the chest wall
DG: EMPYEMA
PLEURAL OCCUPATION BY CYSTS
Young cough, live in the countryside, lung and liver cystic image.
DG: Hydatid cyst
PLEURAL OCCUPATION BY SOLID
Left pleural tumor
Smoking history, work in construction, cough, chest pain
Pleural-based mass, pulmonary Convexity, Location varies
Reduced volume of the hemithorax
OCCUPATION PLEURAL AIR
Recent Pleural tap
Decreased pulmonary murmur
Hipersonoridad
Pneumothorax (spontaneous and traumatic or iatrogenic)
Spontaneous:
Primary:
No previous damage; Bulls apical
More freq. Ho, young, tall and slender, Smokers
Chest pain, sudden shortness of breath.
Medical Treatment:
G1: untreated
G2 and 3: pleural drainage in 5th EI LAM, water trap connected to
Treatment Qx:
Air outlet for drainage> 4 days
Recurrence
High-risk professions
Secondary: Lung damage after: fibrosis, bronchiectasis, emphysema,
asthma, COPD
Treatment: always Qx


Traumatic:
Open:
penetrating wound
Chest wall 1.Missed Calls
2.Traumatopnea
3.Tto immediately: gauze covering the wound, fixed in 3 of its 4 sides.
4.Tto final: chest tube drainage.
5. - Closed: Source: visceral pleura injury or secondary to alveolar hyperpressure sudden chest compression
6.Politraumatizado
7.Tto: if> 20% is drained
8. - A tension: P º intrapleural> P º atm at expiration
9.Mecanismo valve: air gets inspiration / expiration closes
10.Colapso lung, the mediastinum shifts toward the contralateral
11.Dolor, dyspnea, tachypnea, tachycardia, sweating, cyanosis and coughing.
12.Tto: needle in 2nd EI CML
Malignant Mesothelioma
Rare and aggressive malignancy related to asbestos exposure until 40 years ago.
Big capacity that tends to involve invading the pleura widely incarcerated and lung.
Asbestos: common name for a heterogeneous group of minerals called hydrated Mg silicates.
Clinical: chest pain, cough, dyspnea, CEG, massive pleural effusion.
Study and Management
Rx thorax: pleural thickening with large nodules + invasion of the mediastinum.
CT is very useful to differentiate structures.
Pleural effusion: exudation, bleeding gralmente, pH <7.3 (70% cases)
Poor prognosis, survival 6-12 months; rspta bad to chemotherapy and / or radioTx.
Tto: symptomatic palliation.

HEMOPTISIS
removal of blood with coughing, resulting from the hemorrhage of the airway to parenchymal lung structures.
It may be a bloody sputum or exanguinante hemorrhage.
CLASSIFICATION
By magnitude
Mild: <100 ml
Moderate: between 100 and 400 ml
Mass:> 400 ml and for other> 600 ml
Massive Hemoptysis: it is an emergency which if not treated well and in time the patient may die drowning in his own blood
Exanguinante Hemorrhage: Bleeding most 150 ml in one hour for three hours or more acute loss of 1000 ml.
ETIOLOGY
Inflammatory:
Pulmonary tuberculosis, bronchiectasis, pneumonia, lung abscess, Hydatid
Neoplastic:
Primitives:
larynx, trachea, lung, mediastinum
Secondary: lung metastases
Vascular: PTE, mitral stenosis, aortic aneurysm, acute pulmonary edema, arteriovenous fistula, vasculitis.
Hematologic: ITP, Hemophilia Treatment anticoagulant
Trauma transbronchial biopsy, Bronchoscopy, endobronchial foreign body, bruises and wounds.
Other: Endometriosis, Cystic Fibrosis
HOW TO STUDY hemoptysis
Blood pressure, pulse, temperature, blood count, uremia, glycemia, TTPK, prothrombin, ELP, arterial blood gases, and factor group, smear, spirometry.
Bronchoscopy, Ap and lateral chest x-ray, CT chest, bronchial arteriography
The study will depend on the amount of bleeding and the resources we have for research.
POSITIVE DIAGNOSIS
It is based primarily on observation of the physician, whenever possible or by the story told by the patient of removal by blood mouth red sparkling, frothy without food debris and on subsequent days followed by the emission of the dark blood sputum queue called hemoptysis.
DIFFERENTIAL DIAGNOSIS
Hematemesis:
Keep in mind that the blood of the respiratory system can swallowed and then vomited.
EPISTAXIS
FACTITIOUS
CASES
1 .- smoker, 65 years, 2 months dry cough, weight loss, hemoptysis
2 .- A history of repeated pneumonia, abundant expectoration morning,
Hemoptysis daily from 1 month ago.
Massive hemoptysis
They are between 5 and 14% of all hemoptysis. In Chile is estimated at about 8% mortality with medical treatment exclusive 50% and less than 25% when given option of surgery or embolization.

Criteria for poor prognosis
Bleeding greater than 1000 ml within 24 hours, clinical or radiological evidence
aspiration, hemodynamic instability, bleeding of neoplastic
Bilateral pulmonary hemorrhage, pulmonary metastases, Failure to locate the site of bleeding, inadequate pulmonary function
CASE
Chest pain, purulent Bronchorrhoea, weight loss, Alcohol, Hemoptysis

SMOKING
Related deaths of 15-20%, 1 / 3 smokes
IMPACT OF SMOKING
1 preventable cause of morbidity and mortality worldwide
? 3.4% per year (WHO 1999)
Chinese: 1 in consumption = 63% h-4% m
80% smokers start: <18 years
30% of smokers are alcoholics
Antecedent depression 25-40%
WHO 2030: 1 / 3 deaths = snuff, 7 / 10 in developing countries

* 4000 TOXIC SUBSTANCES: 50 carcinogens (particulate)
hidroc.aromaticos hydrocarbons (benzo (a) pyrene), nitrosamines
aromatic amines, benzene, vinyl chloride. Nicotine, co-monoxide, tar, lead, cadmium, toluene, irritants acrolein and NO.
NICOTINE
reward system:
recaptaciónneuronal inhibits dopamine. Dopamine levels, mesolimbicodopaminergico system, nucleus accumbens (prefrontal)
deprivation: inhibits norepinephrine reuptake. gatillaje of
ne neurons. in locus ceruleus
ADDICTION TO NICOTINE DSM-IV
Physical dependence:> 20 cigarettes / day, <30 minutes of waking, difficult abstention.
psychological dependence: modulates mood, habit strength
sx. deprivation:imperative of smoking, anxiety, irritability,
anger, headache, poor concentration, changes in sleep, changes in appetite, dizziness, restlessness
ASSOCIATED DISEASE
90% of lung ca, 15-20% other cancers, 75% COPD, 25% muertescardiovasculares, impactopersonal, family, social, costs, respiratory bronchiolitis, histiocytosis X,> cold, flu, TB, chickenpox,> pneumonia and
Pneumothorax, 2-6 times + complicacionespostoperatorias, 10> mortalidadmaternofetales,> asthma in childhood, early menopause
IMPACT IN PATHOLOGY
ca. lung: 1.10 smoking cig / day ¨ relative risk> 5.5
smoking> 30 cig / day ¨ relative risk> 22
COPD
mac.alveolar, inflammation, injury, matrix, emphysema (r.libres and
Protease ® anti-proteases)
IMPACT ON MATERNAL AND CHILD HEALTH
breathing in utero and lactation nicotine levels = active smoker,
preterm labor,> hiperrreactividad bronchial childhood, children with <FEV1, asthma and more severe development in <7 years
CARDIOVASCULAR DISEASE
snuff and atherosclerosis: dose-response
1 to 4 cig / d triple coronary risk
2.6> iam risk
2-3> bird risk
30> peripheral vascular disease risk
25% of deaths from cardiovascular disease
35-69 (WHO 1999)
BENEFITS ABANDONMENT
> Survival: in <50 years halved the risk of dying in the next 15 years
"Iam-epa-bird at 2 years of cessation
¨ 2-5 years of cessation risk equals the non-smoker
> 10 years of cessation 'lung cancer risk 30-50%
-
Matches FEV1 <operative risk, <child risk, economic benefit

COPD
Limiting chronic, progressive and irreversible airway obstruction (CAO).
With varying degrees of emphysema and airway inflammation
Caused by risk factors such as smoking, exposure to wood smoke or contaminants in the workplace.
CAO "IRREVERSIBLE?
Means a decrease in FEV 1 below the theoretical value, which returns to normal after appropriate treatment, prolonged.
DIAGNOSIS
Suspicion:> 40 years, smoker with chronic cough and / or dyspnea.
Spirometry: obstructive not improved with bronchodilator:
Rx ray: hyperinflation.
Gases: only if FEV 1 <50%.
DIAGNOSIS
Search Physical Examination, Commitment of conscience, Cor pulmonary
Pneumonia, heart failure, respiratory muscle fatigue, hemodynamic instability, deep vein thrombosis,
Comorbidity
RADIOLOGY IN COPD
It may be normal or nearly + / - 50%
Emphysema
Hyperinflation
Oligoemia
Bulls
Increased AP chest diameter
PREVALENCE
USA: 14,000,000 (90% smokers)
Chile:
Bronchial asthma 1.2% to 11%
COPD. ... ... 7.1% to 21% (+ / - 300,000 people> 65 years)
COPD IN CHILE
Hospital discharges:
7,000 annual
Rising mortality rate (persons> 14 years)
1960. ... ... .................. 4 per 100,000
1990 ....................... 20 per 100,000
Chronic medical consultations to determine recurrence, medication use and permanently incapable of work.
Epidemiology
Prevalence - 9.34 male / 1000
- 7.33 Women / 1000
- 52 million people worldwide
Smokers: 14%
Nonsmokers: 3%
Fourth largest killer in the U.S.
DEVELOPMENT OF COPD
Inflow obstruction to the airway by an accelerated decline in lung function 2-5 times normal.
FEV1 ¯ 15 to 30 ml / year
Occurs in 15% of whites and 5% Asian ® genetic differences
Precocious expression in patients with A1AT deficiency who smoke
PATHOPHYSIOLOGY
Reduction: FEV 1 / FVC, FEV 1, FVC, FEF 25-75, V and V máx50% máx75%
Flow rate
Magnification lung capacity. Total Residual volume
Histopathology
Inflammation of the peripheral airways (bronchioles) and lung parenchyma
Bronchiolar obstruction by fibrosis and infiltration by macrophages and lung parenchymal destruction LT ®
LBA: macrophages and neutrophils
leukotriene B4 (chemotactic for neutrophils)
cytokines, TNF, IL-8
MORE RISK FACTORS
Smoking
90% of patients smoke or have smoked
Mortality 15 times> than non-smokers
Fall in FEV1 greater, more dyspnea, and INCAP.
Passive smoking, deficiency of a1 anti-trypsin, Environmental Pollution
HISTORY IN COPD
Home to 40-50 years
History of smoking, TB, severe pneumonia, CF.
Symptoms: Cough and expectoration (90%), dyspnea, chest pain,
Hemoptysis rare in exacerbations, edema of limbs
PHYSICAL EXAMINATION IN COPD
It may be normal at the beginning
Document: dyspnea, pulmonary hyperinflation, respiratory muscle Operation, tachypnea at rest, pulmonary murmur ¯,
Mild cyanosis
EXAMINATION OF PULMONARY FUNCTION
How: Spirometry and GSA
Essential to specify, because:
It is the basis of diagnosis, to quantify the severity of the disease
Reversibility, response to treatment
SPIROMETRY
Airway obstruction, with decreased FEV 1, FVC dismimuída by air trapping, bronchodilator test not significant
If reversed values> 30% suspect asthma
The FEV1 is the index to categorize COPD
Blood gases
Must be completed in all patients studied 1 time
Especially if FEV1 <60%
Moderate hypoxemia
Lifting the Aa oxygen gradient
CO2 sequestration in advanced stages or in acute exacerbations
Staging (GOLD)
0: Spirometry N; cough and sputum.
I: FEV 1 / FVC <70%, FEV 1 ³ 80%
IIA: 80%> FEV 1 ³ 50%
IIB: 50%> FEV 1 ³ 30%
III: FEV 1 <30%
FEV 1 <50% + Insuf. Respiratory or pulmonary Cor.
Staging of COPD
Stage I: FEV 1 equal to or greater than 65% of predicted
Stage II: FEV 1 between 50 and 64%
Stage III: FEV 1 between 35 and 49%
Stage IV: FEV1 less than 35%
FUNCTIONAL CLASSIFICATION
Stage A: FEV 1 ³ 50% (theoretical).
Step B: FEV 1 <50%
TREATMENT PHASE STABLE (EVIDENCE TYPE A)
Current treatments do not modify the natural history of disease.
Muscle training improves exercise capacity and symptoms ¯.
OBJECTIVES:
1.Detener disease progression
2.To improve the quality of life:
¯ Symptoms, physical capacity, prevent exacerbations
3.To improve survival.
TREATMENT PHASE STABLE
1.Cesación smoking
2.Medicamentos: step therapy. Objective: To relieve shortness of breath
a.Etapa A: first step, then the second.
b.Etapa B: specialist
TREATMENT PHASE STABLE
First escalónb2 SOSSegundo escalónb2 2 puff st 6 hours puff c/6Tercer escalónSalmeterol Ipratropium 2.3 Theophylline oral action prolongadaCuarto escalónCorticoide Oxygen

TREATMENT PHASE STABLE
Environmental Management, Immunization, home oxygen, Education,
Respiratory rehabilitation
Treatment in the Steady
Evidence Type A
No rationale chronic treatment with oral corticosteroids.
Respiratory failure: oxygen> 15 hours survival.
Education is essential to manage the illness and quit.
Inhaled steroids in COPD
Decreased frequency and severity of exacerbations
Decreased daily symptoms and medical consultations
Increase walking capacity
They can reduce bronchial hyperresponsiveness
Oral steroids do not predict response to inhaled
Inhaled steroids in COPD
· · Changing
the rate of decline in FEV1
· * Golden S GUIDELINES.
· •
In patients with COPD and persistent symptoms can be tested 3 months with moderate-dose inhaled corticosteroids
· They are particularly suitable for patients with FEV1 <50% and with frequent exacerbations requiring systemic antibiotics and steroids. (more than 1 per year in the last 3 years)
· · PRO: The CI is useful in COPD
Reduces: exacerbations, hospitalizations, symptoms, loss of FEV 1 and
· Mortality
· AGAINST:
The CI is not useful in COPD
· The CI is useful in asthma
· Patients who respond to corticosteroids did not have COPD
· Inflammation of asthma is based on eosinophil
· Inflammation of COPD is based on PMN `s
· PROGNOSIS IN COPD
· Depends on
• The degree of obstruction
· FEV1> 50% ® 75% survival at 5 years
· FEV1 <30% ® <50% survival at 5 years
• The suspension of smoking
• The degree of hypoxemia
·
· EXACERBATED:
· Pathological condition
· Increased dyspnea, cough or sputum that do not respond to standard therapy
· No etiology in 1 / 3 of cases.
Frequency:
· - Non-smoking: 2.4 - 3 episodes / year.
· - Smokers: 5 to 6 episodes per year.
· Exacerbation of COPD
· 1. Increases inflammation / obstruction of the airway.
· Infection tracheobronchial tree, environmental pollution,
· Bronchospasm.
• 2. Decreases gas exchange area.
· Pneumonia, pneumothorax, pleural effusion, pulmonary thromboembolism.
· 3. Extrapulmonary condition that increases the work of breathing.
· Increased metabolic requirements, decreased chest wall compliance and inspired oxygen pressure
· - Cardiovascular: myocardial infarction, arrhythmia, CHF
· HOW SUSPECT Exacerbation?
· Dyspnea, wheezing.
· Volume sputum purulence, fever.
· Thoracic pain.
· Frequency in use of inhalers.
· ¯ exercise tolerance.
· Discomfort, insomnia, sleep or fatigue.
· Depression or mental confusion.
· INITIAL ASSESSMENT: Anamnesis
· Status basal ® Staging
· Characteristics and sputum volume, duration and progression of symptoms, severity of dyspnea, exercise limitation, difficulty eating and sleeping
· Therapy at home, Comorbidity, social status
· · PHYSICAL EXAM FINDINGS
· Prolonged expiration, wheezing Decreases
· Hyperinflation:
· Ribs flattened hipersonoridad, muffled heart tones, suprasternal and intercostal retraction, Hoover sign
· · Use of accessory muscles and abdominal pain, tachypnea, tachycardia;
· Cyanosis,
· Hypercarbia: alt. consciousness edema.
· Pulmonary Cor.
· EXACERBATED FACTORS IN COPD
· Infections, acute bronchitis, pneumonia, respiratory center depression, narcotic drugs, sedatives, oxygen administration
· Respiratory diseases, pulmonary embolism, pneumothorax, pleural effusion, Trauma
· Chest, cardiovascular diseases, CHF, arrhythmias, shock
· Disease Abdominal Surgery, Inflammatory,
· Ascites, systemic diseases, sepsis, metabolic alkalosis
· EXACERBATED: GOALS OF TREATMENT
Identify and correct the underlying cause, reduce work of breathing, respiratory insufficiency Correct, Bronchodilation, adequate oxygenation, antibiotics, corticosteroids, non-invasive ventilation
· EXACERBATED: therapeutic scheme
· Salbutamol:
· ·
4 to 6 puff C/20 minutes for 3 times through a commercial spacer (12 to 18 puff in 1 hour).
· Nebulization of 0.5 to 1 ml in 3 ml of saline (preferred compressed air).
· · - B-adrenergic and anticholinergic:
· FEV 1 and FVC in 15 to 29% (1-2 hrs)
· - Peak: b-adrenergic better.
· - Adverse effects: Ipratropium less.
· - ¯ hyperinflation, dyspnoea and exercise
· Corticosteroids: prednisone 0.5 mg / kg hydrocortisone or equivalent
· Antibiotics (amoxicillin 500 to 750 w / 8 hours, or cotrimoxazole Forte 1 w/12 hours, 7 days)
· Fever, purulent sputum, increased sputum (two of three).
Oxygen therapy:
Hint: saturation <90%
Dose to reach 90%, if not available or gas pulse oximeter, 0.5 to 2 liters per minute
HOSPITALIZATION CRITERIA
Severe decompensation: dyspnoea CF: 4, respiratory muscle fatigue, cyanosis.
Lack of response to treatment in 2 hours, Comorbidity of high risk.
3 consultations in emergency within 48 hours, inadequate social conditions.
CRITERIA FOR REFERRAL TO SPECIALIST
Diagnostic problems, Stage B disease, Cor lung
Indication of oxygen therapy, significant comorbidity, persistent Smoking
PREVENTION
Always ask about smoking in medical office, smoking cessation, Search symptoms suggestive of COPD in smokers, spirometry in smokers> 40 years.
BRONCHIAL ASTHMA
Inflammation, Hyperreactivity, Bronchial obstruction reversible
Fragility of the epithelium that results for its tendency to flaking.
Inflammatory infiltrate composed of eosinophils, lymphocytes (PAF ® muscle contraction, bronchial hyperresponsiveness prostaniodes ®), mast cells.
Increased basement membrane thickness
Hypertrophy of smooth muscle and mucous glands
EPIDEMIOLOGY
It affects 3-7% of the adult population.
In children the prevalence is slightly higher.
Children more likely than girls to develop.
In young adults, the disease affects women more.
Elderly occurs with equal frequency in both sexes.
PATHOPHYSIOLOGY
Eosinophils (leukotrienes ® hypersecretion) and products (major basic prot, prot cationic peroxidase
and neurotoxin) is one of the characteristics of asthma
Increased training in the bone marrow, the mucosa Attraction to cytokines and chemotactic factors adhesins, activation in situ to release their products
Mast cells (histamine ® edema)
CHEMICAL MEDIATORS
histamine (bc)
Eicosanoids
cyclooxygenase:
PGE2, PGF2a, PGD2, thromboxane
lipoxygenase: leukotrienes (BC) slow-reacting substance of anaphylaxis
Platelet activating factor (BC)
ATOPIA
Hereditary condition: excessive immune response: increased production of IgE against environmental substances.
Abnormality on chromosome 11: IgE synthesis exaggerated x the LB turn regulated x CK IL4 (TH2) and INF-ã (TH1).
IgE and other CK activated eosinophils and mast cells that release chemical mediators: smooth muscle contraction, edema and hypersecretion: bronchial obstruction.
HYPERSENSITIVITY immediate and late
Inhalation of allergen x asthmatic sensitive to that of bronchial obstruction after 10-15 min and improves after 30-60 min.
In some jet late hours later to develop more slow and long.
Immediate reaction to partially prevented by antihistamines, adrenergic and sodium cromoglicolato.
The latter and the GCC can prevent the development of the slow response.
HYPERREACTIVITY BRONCHIAL
Excessive tendency against bronchoconstrictor stimuli
Can be assessed by chemical stimuli (methacholine, histamine) or physical (exercise, hyperventilation).
The degree of hyperreactivity against methacholine or histamine is correlated with asthma severity.

Image

Intermittent asthma
Dyspnea with wheezing of varying intensity, asymptomatic periods, predominance in childhood, causes allergic or not, Variable intensity of crises, difficulty in inspiration, good prognosis
Persistent asthma or chronic
Continued presence of cough, wheezing, breathlessness and oscillating and variable intensity increases at night, adulthood, viral etiology, symptoms are consistent with climate change, state of mind, existence of environmental irritants. Worse prognosis
Asthma atypical
Persistent cough with wheezing, dyspnea, chest tightness, bronchial obstruction reversible with bronchodilator

DRIVERS
Allergy, Occupational asthma, Exercise and hyperventilation, infections, emotions and personality, Medicine, gastroesophageal reflux, menstruation and pregnancy
THERAPEUTIC APPROACH
Preventive: exp. Triggers
Pharmacological:
Antiinflammatory: Nedocromil sodium, glucocorticoids
Bronchodilators: B-mimetics, methylxanthines, anticholinergics
INFLAMMATORY
Nedocromil / Cromolyn Sodium
Preventive action
No bronchodilator
Moderate effectiveness
Nedocromil: only INH
Dose: 2-4mg / 6-8h
Cromolyn: 4 cap 20mg / 24h
Hint: background tto moderate persistent asthma
Glucocorticoids
Preventive action
Oral: Prednisone and Prednisolone
Full cycle: 30-40mg/24h 2 or 3 days gradually decrease 5 mg/2dias
Cycle length: 30-40mg/24h 7 to 10 days
Indication: severe persistent asthma
Via inh: beclomethasone and budesonide
Rare efect.secundarios
Dose 400-800mcg/24h
Key to effective preventive action in regular use without bronchodilator effects
Dose: 1 inh/12h (up to 3 or 4/day)
Via IM / IV: 6metil-prednisolone and hydrocortisone
Ind: Worsening severe asthma
Bronchodilators
B2miméticos
Short-acting (Max 15): Salbutamol, terbutaline, and fenoterol carbuterol.
6-hour duration of effect Via adm: Aerosol.
Note: When there is clinical.
Next exposure to known triggers.
Take continuing can increase nonspecific hyperreactivity
Longer-acting salmeterol and formoterol.
12 h. Duration of effect
Moderate or severe asthma not controlled with inhaled Gc.
Methylxanthines: Aminophylline and theophylline
½ life variable (8h adults, children 4h).
Optimal plasma concentrations: 5 to 25 mg / l.
200 mg/12h oral dose, with increments of 100 mg.
Controlling levels> 400-500 mg/12h.
Ipratropium bromide: a similar effect but with home mimetics B2
slower. Of choice in chronic bronchitis and emphysema
TREATMENT
Mild:
Mild symptoms and limit physical activity esporádicos.No
Normal CV intercrisis;? 4 inhalations / week
* Demand inhaled B2 agonists
Moderate: Mild symptoms but frequent (2-3/sem).
S. sporadic intense, easily triggered.
CV most affected. Almost daily inhalations.
* Inhaled glucocorticoids (200 - 250 mcg/12h) or Nedocromil
sodium (2-4 mg/6h)
- Good answer: inhaled glucocorticoids (200 - 250 mcg / day)
- Poor response: inhaled glucocorticoids (600 - 750 mcg / day)
(Add B 2 inhalers if symptoms)
Severe asthma;
Full cycle
Gc oral: 30-40 mg/24h/2 or 3
Gc inhaled: 800-1000 mcg / day
Gc inhalados.1200-1600mcg/día
Gc inhaled: 400-500mcg/día
Gc inhaled> 1000mcg/día, maintenance
B 2 agonists long-term
Theophylline and / or ipratropium bromide
Inhaled Gc> B 2 agonists 2000mcg/día + long term +
Theophylline + ipratropium bromide
Oral Gc


ARDS, EPA, chronic cough
EPA (Acute Pulmonary Edema)
Cardiogenic, No cardiogenic Myocardial Pump Failure
PATHOPHYSIOLOGY
Increased retrograde hydrostatic pressure which creates difficulty in left ventricular emptying and congestion, increased permeability of abnormal pressure in arterioalveolar discover our exclusive special, flood the alveolar space, intrapulmonary shunt
CAUSES
Non-cardiogenic: ARDS
Cardiogenic: Heart failure, myocardial infarction, valvular disease, cardiomyopathies
TREATMENT
Compensation: Preload, contractility, afterload
Preload: Limiting tidal volume, Measuring central venous pressure, pulmonary capillary wedge pressure measurement
Contractility: Improve the basic cause, thrombolysis, vasoactive drugs, balloon counterpulsation, mechanical ventilation
Afterload: Diuretics, Lower Blood Pressure
FORECAST
Cause of death in terminal chronic congestive heart failure
good prognosis in acute hypertensive crisis event without myocardial failure
poor prognosis in acute event associated with myocardial failure
ARDS
Pulmonary Edema from non cardiogenic Permabilidad Increased pulmonary capillary, severe respiratory distress with Intrapulmonary Shunt, triggered by a condition or risk factor predisposing
DEFINITION
acute respiratory failure, bilateral pulmonary infiltrates, severe hypoxemia, absence of cardiogenic origin EPA
IMPACT
13.5 per 100,000 population per year
Incidence of ARDS in patients admitted to ICU ® 4 to 15%
RISK FACTORS
Pulmonary aspiration of gastric contents, pulmonary infection, drowning, chest trauma, inhalation injury
Extrapulmonary: sepsis, severe non-thoracic trauma, shock, Politransfusiones, fat embolism, Acute Brain Injury
PATHOPHYSIOLOGY
Macrophages, proinflammatory cytokines, interleukins, Tumor Necrosis Factor, inflammatory response, edema fluid passage to the alveolar space
PATHOPHYSIOLOGY
Early Phase
Late Phase
Intrapulmonary Shunt
V / Q = 0
FORECAST
mortality between 40 and 60% die from multiple organ failure, predictors of mortality, severity at admission
organ dysfunction, severe pre-existing diseases, age,
Shock and Severe Sepsis
CHRONIC COUGH
Leading cause of consultation in primary care and specialty
Etiology groups from banal diseases (cold) until death (cancer)
On diagnosis of acute bronchitis, a millionaire in self-medication expenditure

Acute cough: lasts <3 weeks
Common cold, acute rhinitis, acute sinusitis, exacerbation of COPD
Acute Cough Common Cold
Nasal symptoms: nasal congestion, rhinorrhea, sneezing, post-download
With or without fever, pharyngitis, normal examination, spontaneous evolution
Acute Cough Rhinitis
Nasal symptoms: nasal congestion, rhinorrhea, sneezing, post-download
No fever, with a history of atopy, pale nasal mucosa
Treatment: antihistamines, steroids
Cough Acute Sinusitis
Nasal symptoms for> 10 days: Nasal congestion, rhinorrhea, sneezing, post-download.
Feeling of facial flushing, stuffy ears, history of rhinitis, purulent nasal discharge and pharyngeal Sometimes halitosis and dental pain
There is always fever and facial pain
Rx CPN: (sensitivity 60 to 70%): fluid level, total opacification, mucosal thickening> 3 mm
* Air-fluid levels in maxillary sinuses


Treatment: (acute sinusitis)
More oral decongestant pseudoephedrine ® antihistamine, topical nasal decongestant, and investigate the chronic use of rebound phenomena
Antibiotic for 3 weeks ® H. Influenzae, and S. Pneumoniae

Subacute Cough (duration> 3 weeks and <2months)
Aetiologies Post infectious, acute sinusitis, bronchial asthma
Cough Subacute Infectious Post
Table report: It begins as IRA, Improvement anything but cough, normal physical examination, no history of similar tables
Exams: normal chest x-ray and CPN
Treatment: codeine, anticholinergics, bronchodilators, corticosteroids, systemic / topical
Sinusitis Subacute Cough by
Similar to that described Clinic
Indispensable complement to imaging study (CT - CPN)
Discard obstructive drainage phenomena CPN
Subacute cough for Asthma
Table report: Obstruction is repeated periodically, coexists with rhinitis and sinusitis, atopic Background
Review: There may be wheezing, variable PEF
Treatment: B2 (+), and inhaled corticosteroids

Chronic coughs last> 2 months
Rear discharge syndrome
(> 95%)
- Rhinitis and Sinusitis
Asthma, GERD, COPD, Drugs, Bronchiectasis
Respiratory Syndromes (? 5%)
Many etiologies, Graves (cancer), infectious, noninfectious
Reversible / non-reversible.
SYNDROME AFTER DISCHARGE
Rhinitis and Download Post
Search for nasal symptoms, history of atopy, gatillantes (pollen, labor),
Signs and symptoms of post-discharge, chest X-ray always, and CPN
Treatment described
Download and Sinunitis Post
They have no diagnostic test, suspected by history and examination, treatment with antihistamines, corticosteroids and / or anticholinergic nasal, always discard Sinusitis
Asthma Chronic Cough
The cough may be the only symptom
Routine diagnosis: Clinical, spirometry, PEF, Rx Tx clean Methacholine: more false positives
Treatment: If in doubt, is treated as asthma for 1 to 3 months, and evaluated
Chronic Cough: RGE
Second or third in the list of common diagnoses
Mechanism: aspiration, laryngeal stimulation, and stimulation in distal esophagus
± 40% do not have symptoms of GERD, diagnostic confirmation is slippery
Chronic Cough: COPD
First stage of COPD: 0: risk, cough and sputum production, normal spirometry
Diagnosis by history, spirometry and normal T Rx
Treatment: stop smoking, B2
Chronic cough: Medicines
Enalapril: blocking angiotensin converting enzyme ® bradykinin
Incidence 3 to 20%
Cough starts a week, and goes from 1 to 4 weeks or persist indefinitely long list of drugs (B-blockers), Search dirigidamente always
Chronic Cough. CXR
If the chest X ray is normal think: Allergic rhinitis, nonallergic, and vasomotor, chronic sinusitis, asthma, GERD, Medicamentosa
If the chest X ray is normal not think about: bronchogenic cancer, tuberculosis, sarcoidosis, bronchiectasis
COMPLICATIONS OF COUGH
Cardiovascular: syncope, hypotension, bradyarrhythmias
Neurological: cough syncope, poultry, headache, seizures
GI: GERD, hernia, or gastrostomy malfunction of sny
Genitourinary: incontinence, urinary incontinence, genital prolapse
Musculoskeletal: rib fractures

DRUGS FOR HYPERTENSION (HT)
 - BLOCKERS
â receptor antagonists - adrenergic receptors: effect decrease cardiac output, release of renin, sympathetic activity, reducing myocardial oxygen consumption
selective A1 ® atenolol, metoprolol (lower risk of broncocontricción)
A1 A2 ® nonselective propranolol, alprenolol


INDICATION
Hypertension, supraventricular cardiac arrhythmias, myocardial infarction secondary prevention, hyperthyroidism, migraine prophylaxis
CONTRAINDICATION:
- COPD, peripheral arterial insufficiency, bronchial asthma - MAO blocker use, IC, AV block 2nd and 3rd
DOSAGE
1 - propranolol: Adults: 10-80mg/dosis. Orally every 8-24h.
2 - atenolol: Usually 100mg/day. Oral 1-2 tablets every 12-24 hours.
OVERDOSE: required emergency hospitalization, life is at risk
Channel antagonist CA + +
General Action: Calcium channel antagonists type voltage regulated by the union through the á1del channel subunit. effect on arteriolar smooth muscle relaxation occurs genral level and decreased cardiac inotropism.
heart action: fenilaquilaminas (verapamil)
smooth muscle action: dihydropyridine (nifedipine, amlodipine)
Intermediate action: benzodiazepines (diltiazem)
INDICATION
Hypertension, angina pectoris, myocardial infarction treatment, supraventricular tachycardia, carotid atherosclerosis
CONTRAINDICATION
AV block 2nd and 3rd, congestive heart failure
DOSAGE
1 - NIFEDIPINO: Adults: 10-20mg/dosis. Oral every 6-8 hours or every 12 hours for extended-release tablets LP.
OVERDOSE: hipotención produced, altered consciousness, coma, hypoxia, requiring hospitalization
Blocker - ADRENERGIC
nonselective and selective antagonist of receptors A1 - A2: have the effect of vasodilatation and decrease of blood pressure, lowers LDL and increase HDL.
Non-selective antagonists: Phenoxybenzamine, phentolamine (not used for its effects on arrhythmias and tachycardia)
Antagonists selective A1: Doxazosin, terazosin (used for: HTA)
NOTE:
Hypertension, pheochromocytoma, benign prostatic hyperplasia
CONTRAINDICATION:
orthostatic hypotension, congestive heart failure
DOSAGE
Terazosin-DOXAZOSIN: 1 mg / day preferably at night, increasing to 2mg/día after 1-2 weeks, depending on patient need to no more than 8mg/día
OVERDOSE: If hypotension occurs, place the patient supine with the head down and apply symptomatic treatment
ACE INHIBITORS
Zn atom binding (ACE active site) and the leucine molecule c-terminal of Ang I, decreases resistance vessels, reduces cardiac load, decreases in BP, decreases aldosterone.
Drugs:
1 - enalapril, lisinopropil, ramipril, perindopril, trandolapril, captopril
2 - losartan (ANG.II receptor antagonist)
NOTE:
HTA, IC, after myocardial infarction, diabetic nephropathy, renal failure
CONTRAINDICATION:
Pregnancy, renal artery stenosis, hyperkalemia
DOSAGE
Enalapril
5 to 40 mg
/ day in 1 or 2 divided doses Start with 5mg 1 time per day, increasing slightly, depending on response.
Reduce by half the dose in patients with renal insufficiency.
OVERDOSE: can cause shock, kidney failure, hyperventilation, tachycardia, dizziness. treated with saline, and if it is recent, gastric lavage
SIDE EFFECTS:
Cough, hypotension, i. renal (stenosis), hyperkalemia
DIURETICS
direct and indirect action on the renal filtrate. loss effects are active and selective reabsorption of solutes (NaCl - NaHCO3) and water
Drugs:
1-loop diuretics (transporter Na / K/2CL, RAAH): furosemide, piretanida, torasemide,
2-thiazide diuretics (transporter Na / Cl, TD): bendrofluazide, hydrochlorothiazide, ciclopentazida, indapamide, xipamide, chlorthalidone
3 - spironolactone (aldosterone antagonist)

4-triamterene, and amiloride (CT, DC, blocks Canalda K Na excretion decreases and increases ac. Úrico)
- Potassium-sparing
NOTE:
Hypertension, heart failure, kidney failure (asa), post heart attack (aldosterone blockers)
CONTRAINDICATION:
drop (thiazides), kidney failure - hyperkalemia (anti-aldosterone), pregnancy (thiazide)

DOSAGE:
1 - furosemide (ASA): As an antihypertensive, 40mg twice daily. Maximum: up to 60mg daily. Children: 2 mg / kg in one dose or increase the dosage 1mg to 2 mg / kg every 6 to 8 hours to obtain the desired response
2 - chlorthalidone (thiazide): Antihypertensive: 25 mg to 100 mg / kg / day for 3 days a week
3 - spironolactone: Antihypertensive: 50mg to 100mg once daily in 2 to 4 divided doses for 2 weeks.
Maintenance: Adjust dose according to individual patient needs
OVERDOSE: depends on the patient, may require hospitalization or symptomatic treatment.
SIDE EFFECTS:
Hipopokalemia,
metabolic alkalosis (exit H), gout (thiazide), hypovolemia, hyperkalemia (PR), metabolic acidosis (retention of H)

HTA TREATMENT
* Urgency HTA: In the absence of target organ damage prefer mouth.
Clonidine: centrally acting agents, vasoconstrictor tone decreases in heart, kidney and peripheral vasculature, works by stimulating postsynaptic alpha adrenergic receptors in the medulla, studies show its effectiveness in lowering BP effectively.
Nifedipine: non-significant reduction in cerebral blood flow, minimal adverse effects.
Captopril: Few studies have assessed their use, orthostatic hypotension in the first dose.
Labetalol: Alpha and beta antagonist, no differences between 100, 200, 300 mg
Conclusions:
Nifedipine the most studied and therapy of choice.
Clonidine very effective, but with prolonged time of action.
Labetalol, a few studies, safe drug.
Captopril no choice.
There is no evidence of benefit of immediate reduction in BP in the absence of target organ damage.
Prefer a gradual reduction in days to weeks
* Emergency hypertension: BP should be reduced to prevent progression
organ damage, always maintain organ perfusion
appropriate, maximum 25% Decrease in MAP, with continuous monitoring parenteral medication in the ICU.
Nifedipine can be used orally.
Nitoruprusiato
: The most powerful, predictable and faster action, minimal effects on CNS, ANS, TGI and smooth muscle, there are no comparative studies to date, Vasodilator Joint (arterial and venous)
Diazoxide: direct arterial vasodilator, effective in 90% patients, its use has decreased by severe hypotension.

Treatment specific situations.
AVE:
Caution in reducing cerebral hypoperfusion due to peri-infarct areas.
Sudden drop in BP can decrease cerebral blood flow and worsen the neurological deficit.
Only introduce antihypertensive TTO: Evidence of other organ damage, encephalopathy hypertension, diastolic BP> 130.
Dealing with short half-life drugs, preferring Nitruprusiato.
Aortic dissection
The risk of progression is directamenteproporcional with the TA.
Nitroprusside use more b-blockers, no data exist comparing the relative efficacy of these agents.
Hydralazine Diazoxide or not use it cause reflex tachycardia.
IAM:
Do not use drugs that cause reflex tachycardia by increasing consumption
oxygen by the myocardium.
Prefer to nitroglycerin nitroprusside (reduces myocardial blood flow in areas of coronary stenosis).
Dar b blockers without not contraindicated.
Pregnancy induced hypertension:
Magnesium sulphate in eclampsia indicated. Prevention and management.
Effective antihypertensive, no significant differences between Labetalol and
Hydralazine in the management of pregnancy-associated hypertension
ACE inhibitors contraindicated.
Pheochromocytoma:
Ppalmente HTN is caused by alpha adrenergic stimulation.
Preferred alpha-adrenergic blockers, b blockers do not use without associating with
alpha blockers
Alternative labetalol and nitroprusside
Scleroderma Renal Crisis:
Associated with malignant hypertension
Renin activity and angiotensin II levels.
The Captopril is the drug of choice.
Survival of 76% per year treated vs 15% not treated with Captopril.

VALVE DISEASE
Commitment heart valves, variable: severity, type of presentation, etiology, behavior, and myocardial involvement
treatment.
Univalvular v / s multivalvular
High incidence? enf. Rheumatic
CLASSIFICATION
Type of Injury: stenosis, insufficiency, mixed.
Affected valve: Mitral - Aortic
Etiology: Enf. rheumatic degenerative processes, congenital pathology
Release Form: Chronic v / s acute
Deleterious effect caused by the hemodynamic condition of the myocardium. Forecast.
Acute: IC ag, progressive course and poor prognosis
Hemodynamic effects of valvular lesions
Stenotic lesion
Pressure gradients during the cycle phase in which the blood flows through the valve.
Turbulent flow, not laminar? ä proportional to pressure.
The severity was assessed according to the valve area.
There must be a 50% reduction in valve area to transvalvular gradient is detected.
Injury insufficient:
Volume overload in both chambers, the behavior varies according to valve.
Ins. Year:? the volume and pressure secondarily.
Ins. My: reduce afterload and single overload
volume.
Effects depend on the volume regurgitated HMD and camera that receives the flow.
Mixed lesions.
Except for a severe commitment or other injury.
From the anatomical point of view
DIAGNÓTICO
Anamnesis
Physical Ex?
valve type, severity, systemic impact
ECG: suspicion does not exclude a valve Normal
ECO - DOPPLER:
Details the lesion, severity, impact on the cardiac chambers.
Ventricular function, pulmonary pressures on land, other injuries, determines response to tto., Evaluates the progression of the painting, is operator dependent, is dependent on the quality of the image.
Chest X-ray. Global Assessment of heart size, observed features and relationships of the aorta.
Estimated impact on pulmonary territory
EPIDEMIOLOGY
In developed countries the incidence has declined by enf valve. rheumatica.
Degenerative lesions: myxomatous and fibrocálcica.
In Chile, a situation of transition.
Mitral Stenosis
Late complication of rheumatic disease (> 95%)
Female predominance, Involvement of the entire valve apparatus
Chronic inflammation with fibrosis, retraction, and even fusion of calcification.
Reduces valve area (N: 4 to 6 cm2)
Infundibuliforme aspect, progressive disease
Growth of left atrium
PATHOPHYSIOLOGY
Resistance to drainage of the left atrium, diastolic pressure gradient, systolic disorder: a decrease in preload (VI)
Diastolic disorder: elevated left atrial pressure.
Important in early diastole, and diastasis lower on rise again in presystolic period by atrial contraction.
It also increases the gradient for? Filling time? ? in pulmonary capillary pressure
Difficult to increase the debt
Developmental stages
There is only the beginning? the gradient against last year.
The more severe: pulmonary vascular complications. (Area <1 cm2)
Elevated pulmonary artery pressure, hypertrophy and dilated right ventricle with secondary tricuspid ins.
Paradoxical fall in pressure in the pulmonary capillary territory.
CLINIC. HISTORY
Appear 5 or more years after the outbreak corea.Secundarios rheumatic or the left atrial hypertension and pulmonary congestion, pulmonary capillary hypertension in situations that increase the heart rate or capillary flow. (Anemia, pregnancy, exercise, FA, fever, hyperthyroidism)
- Dyspnea, EPA, hemoptysis, decreased physical capacity, right heart failure: visceral congestion, abdominal pain, anorexia, fatigue.
- Anginal type pain associated with HTTP and overhead vent. Right.
- Reduces the severity of dyspnea and rapid fatiguability appears low cardiac
Systemic emboli lodged in left atrial thrombi.
CLINIC. EX ASIC
Manifestations depend on the severity of the stenosis
Mitral flap, a sign of low cardiac output, arterial pulse inconspicuous, low amplitude, the low cardiac (carotid)
In precordium, wide pulse and sustained right parasternal. Overload
Diastolic thrill in the left lateral.
1R intense, snap closure, 2R http intense, Noise of openness valve opening snap
Diastolic murmur presystolic reinforcement ferries, crescendo and decrescendo.
Congestive signs in lungs, hepatomegaly, edema.
DIAGNOSIS
ECG:
left atrial size or FA.
RX Chest: pulmonary vein cephalad redistribution, Kerley lines, edema, fissures, EP, growth left atrium and right ventricle.
ECO - Dopppler: Confirms. Very sensitive; Veils thickened, stiff movements and diastolic dome formation. Veil continues the previous post.
Veils, rings and more echogenic and subvalvular apparatus can be merged.
In the short axis two-dimensional echo is measured valve area and there observed the fish mouth appearance in the mitral.
Estimated pulmonary artery pressure, and presence of atrial thrombi.
INVASIVE STUDIES
You can omit if you have other associated valvular or coronary disease presumption.
DIFFERENTIAL DIAGNOSIS
CIA confusion of a widely split second sound with crack. With ferries ferries mitral tricuspid
TREATMENT
It depends on the degree of stenosis, according to symptoms, tto Conservative or not, surgery, surgical mitral valvuloplasty, percutaneous balloon valvuloplasty catheterization and right atrial septum perforation IA. Inflating the balloon at the valve which allows opening.
Indications: symptomatic mitral stenosis, valve area less than
1.5 cm2.
Success: 50% increase in valve area.
CI: significant mitral regurgitation; mobile Intracardiac thrombus.
Complications: Perforation fibrillation; left ventricular perforation. Stricture residual mitral regurgitation secondary.
Syncope, arrhythmias.
Tto conservative Beta ® lock to control the FC; digitalis
If FA; Prevention of rheumatic disease and endocarditis
infectious.
Mitral insufficiency
Incompetence of the mitral valve annulus dilation, rupture or dysfunction of veils or subvalvular apparatus.
Enf. rheumatic veil and cord retraction
Enf. myxomatous prolapse and ruptured cord veils tendínea
Ischemic heart disease: rupture or papillary dysfunction demúsculo
Infective endocarditis: perforation of veils and broken strings.
Myocardial damage: mitral annular dilation
FISIOPATLOGÍA
Regurgitation of LV ejection volume of the left atrium.
Left atrial overload and low resistance to emptying of the left ventricle
Elongation myocardial hypertrophy eccentric mounting Volumes VI, with impaired ventricular function and left atrial hypertension.
Volume and pressure overload in AI.
CLINICAL
Pulmonary congestion, dyspnea, PND, orthopnea.
GC insufficient fatigue, emaciation
HTP: right ventricular failure, visceral congestion.
Cardiac Exam: apexiano systolic thrill.
No decreased 1R, 2R N or increased, 3R (+)
Systolic murmur: holosystolic. Also proto and TV. Irradiation to armpit and back.
EVOLUTION
Slow progression with good tolerance and symptoms in relation to effort or intercurrent events (upper respiratory infection, FA)
Poor prognosis when stronger signs of left ventricular failure.
Mitral insf acute infective endocarditis, rupture of subvalvular apparatus or valve myxomatous ischemic.
Signs of pulmonary congestion and low cardiac output.
DIAGNOSIS
VI Growth and 3R
ECG: growth of the left atrium and ventricle
Rx Chest: pulmonary changes and growth of cardiac chambers.
Eco - Doppler crec level AI and VI volume overload, etiological diagnosis, important for the therapy.
Study invasive coronary heart disease associated LV function, filling pressures and Ai VI, pulmonary pressures
TREATMENT
In the case of chronic adaptation mechanisms are hardly correctable
Preveción of infective endocarditis and FR Restriction of physical activity; vasodilators (ACE inhibitors, hydralazine), increase the effective stroke volume.
Salt restriction and diuretics, digitalis, before myocardial injury Valvuloplasty
Echocardiographic end-systolic diameter <45 mm, tto doctor,> 50 mm surgical tto
Diam intermediate, according to clinical decision.
Aortic Insufficiency
It mainly affects men
Etiology:
Enf. Rheumatic (60%), infective endocarditis, aortic dissection, annular dilatation (aneurysm, hypertension), Traumatic rupture
PATHOPHYSIOLOGY
VI reflux into a% of volume ejected. Doblellene ventricular
? diastolic and systolic vol vol. Increased pre-and afterload VI. LV hypertrophy
CLINICAL
Side: Increased volume and cardiac ejection volume, coronary insufficiency, heart failure, palpitations and mov. chest, angina, dyspnea, orthopnea, PND, EP, CCI.
EX. ASIC
Dance blood pressure increases by beating amplitude, rise and fall quickly.
Hypertrophy and dilation of VI
No decreased 1R, 3R (+)
Mesodiastólico and early diastolic murmur, Austin Flint ®.
Systolic murmur due to increased systolic ejection volume
EVOLUTION
Years asymptomatic Appearing as evidence of hypertension
Px left atrium with severe failure of the LV contractile
In the case of acute Ao Ins, there is an initial period when the ventricle fills the peripheral demand. Rapid progression. Sx of pulmonary comngestión GC after insufficient.
DIAGNOSIS
ECG: left ventricular hypertrophy.
Diastolic overload (initial change) and systolic overload.
Rx thorax: VI enlarged, dilated ascending aorta, AI growth and changes in the pulmonary circulation.
Eco - Doppler evaluates dilation and hypertrophy of VI.
Mitral flutter, Diagnosis of aetiology.
TREATMENT
Preventive measures before the onset of Sx., Newspaper Control, Prevention of infective endocarditis and ER, heavy physical activity limitation, arterial vasodilators, valve replacement, durability and thrombogenicity. Early symptoms or increased pressure of AI. VI with progressive dilation
Diam systolic less than 40 mm, without indication, surgery before the diameter reaches 55mm
Aortic stenosis
Home etiology: congenital
PATHOPHYSIOLOGY
Thickening and fibrosis of veils, with reduced opening during systole, increased afterload, concentric hypertrophy
Good valve function with diam greater than 0.8 to 0.9 cm2
Pressure gradient between aorta and VI during the
systole.
CLINICAL
Symptoms with valve orifice smaller than 0.6 to 0.7 cm2
Around age 50,
Angina: balancing between irrigation hypertrophy and coronary
Dyspnea of effort, increased diastolic VI P °, decreased compliance x hypertrophy and impaired contractility.
Syncope of holistic efforts.
EX. PHYSICAL
Tardus et parvus pulse pressure, decreased amplitude and promotion.
Carotid pulse slow ascent with systolic murmur and thrill. Good indicator.
Left ventricular hypertrophy. Clash of the tip.
Click ejection after 1R, 4R, 3R, if it is lacking ventricukar.
2R paradoxical Desdoblamineto
Systolic ejection murmur that was heard at the apex, left sternal border, 2nd right intercostal space, radiating to the neck.
EVOLUTION
Asymptomatic for long periods, Poor prognosis to become symptomatic
Survival of 2 to 3 years after syncope anginao and less than 2 years if ICC.
FA, less common but decompensation.
DIAGNOSIS
ECG: ventricular hypertrophy sobrecaga sistólica.Frecuente LBBB
Chest X-ray: concentric hypertrophy: low dilation of cavities. Dilation of the aortic root calcifications.
ECO-Doppler hypertrophy. Veils; vascular gradient estimate.
TREATMENT
Prevencción EI, ER, Regular Monitoring
Significant stenosis> 50 mmHg asx, control
Significant symptomatic stenosis: Surgery of valve replacement, balloon valvuloplasty is most common in children.

Thyroid disease
Hypothyroidism: increased TSH, free T4 decreased, feeling cold, ragged Language, Weight gain, Bradisiquia, depression, brittle hair, constipation
Hyperthyroidism: TSH almost undetectable,Increased free T4, sensation of heat, nervousness, weight loss with preserved appetite, resting tremor, irritability, diarrhea
Asymptomatic euthyroid
Nodule
Goiter
THYROIDITIS
Inflammation of the thyroid gland
It includes a diverse group of diseases that clinically present with increased thyroid volume and thyroid function changes.
Not infrequently the patient passes through different states of thyroid function.
Different approaches depending on the etiology
CLASSIFICATION
Etiologic:
Autoimmune thyroiditis, or posviral viral, bacterial or fungal suppurative (specific or not), and postradiation thyroiditis associated with granulomatous diseases such as sarcoidosis.
Form of presentation:
Acute, subacute or chronic, Postpartum Tiroidistis silent or painful, their histological features:
Granulomatous (subacute), Lymphocytic, oxyphilic or fibrous
According to the time course and nature of these in:
1. Acute
2. Subacute: granulomatous (De Quervain), Lymphocytic, Sporadic. (Silent), Postpartum
3. Chronic Lymphocytic
CLINICAL
Clinically, autoimmune thyroiditis and postpartum are usually painless, although its presentation may be acute or not.
Infectious thyroiditis, viral and postradiation are painful and acute presentation.
Patients with viral thyroiditis, autoimmune postpartum and may present clinical manifestations of thyrotoxicosis, with hypothyroidism or
present with euthyroid goiter.
Suppurative thyroiditis are rare.
There is local pain involving the entire gland or part of it, making the general statement and sometimes fever.
THYROIDITIS
Acute
Very rare, 20-40 years
Bacterial: Streptococcus, Staphylococcus, Salmonella, Mycobacterium
Tuberculosis.
Fungal: Candida, Aspergillus, Mucor
Postpartum
Frequently, 10% of pregnant women.
Begins between 1 and 6 months after delivery.
Hashimoto's thyroiditis
Most common cause of hypothyroidism in the
areas where there is dietary iodine deficiency.
Major cause of non-endemic goiter
It is characterized by gradual thyroid failure secondary to immune destruction of the thyroid.
It represents a diffuse goitre leading to progressive destruction of the follicular epithelium which can lead to hypothyroidism
Epidemiology: 45-60 años.Mujeres 10:1
HASHIMOTO
Etiopathogenesis
Familial aggregation, association with HLA-DR3.
? There are antibodies against antigens of the follicular epithelium, default on the role of specific suppressor T cells of the thyroid
Clinical:
It mainly affects postmenopausal women, glandular enlargement.
Elevated T3 and free T4, TSH low.
DIAGNOSIS THYROIDITIS
Clinical and complementary tests:
Leukocytosis with left shift and increased in cases of VHS suppurative and subacute thyroiditis.
ECO tioridea showing the thyroid abscess in cases of suppurative thyroiditis.
In the fibrous form, there is a generalized hypoechoic pattern.
131I uptake decreased, especially in subacute thyroiditis and irregular pattern in the fibrous form of autoimmune thyroiditis.
Fine needle biopsy: in most cases allows the diagnosis by demonstrating the pus (also serves to obtain sample for culture and sensitivity).
Thyroid function tests can confirm or not the presence of dysfunction.
TREATMENT
Suppurative thyroiditis:
Specific antibiotics, drainage.
Subacute thyroiditis:
During the phase of thyrotoxicosis, it is suggested to use GC (30-40 mg / day of prednisone) or NSAIDs and propranolol (60-80mg/día).
During the phase of hypothyroidism using levothyroxine sodium (2.5 ìg / kg / day), average 6 weeks.
If the patient does not tolerate the associate suggested suppressive dose propranolol in low doses.
At the end of the period of time under suppressive treatment, you are advised to remove the thyroid hormone and assess the state of thyroid function, which will be indicated for TSH and free T4 after 2 weeks to determine if there is recovery.
Autoimmune thyroiditis:
Levothyroxine sodium, a drug that is indicated for life.
In the nodular variant, also indicate the levothyroxine sodium and follow-up will be similar to that for euthyroid multinodular goitre.


Postpartum thyroiditis, silent thyroiditis:
Require treatment with propranolol in doses between 60 and 80 mg / day during the phase of thyrotoxicosis or levothyroxine sodium during the phase of hypofunction.
In general, the treatment scheme is similar to subacute thyroid.
PROGNOSIS (thyroiditis)
Excellent, no cases of recurrence and postradiation suppurative thyroiditis, although the latter may be hypofunction
final.
Recurrences in cases of subacute thyroiditis de Quervain.
Final hypofunction in postpartum thyroiditis, silent thyroiditis and autoimmune forms.
EPIDEMIOLOGY
Most common malignancy Endocrine System
Low Frequency: 1% of all Ca
Higher prevalence in women, tends to equalize after the 5th decade
Presence of a thyroid nodule in men involves three times higher risk of cancer
Age of presentation: Between 25-65 Years, Peak at 40 years, has been an increase in papillary carcinoma, with decreased follicular and anaplastic types, Single Ca that lymphatic invasion is not
necessarily malignancy
FACTORS PREDISPOSING
Only known factor:
ionizing radiation in cervical region
Risk Factors: Women, Race Asian History fliar, hyperparathyroidism, benign diseases (TSH
Persistently high)

THYROID CANCER
The most common symptom of thyroid cancer is a nodule
The only way to know if a lump is cancerous or not is to test (puncture with a needle biopsy or removed).
The treatment of thyroid cancer is usually surgical, unless it already has spread to other parts of the body.
CLASSIFICATION OF THYROID TUMORS
Primary epithelial
Follicular cells:
Benign follicular adenoma.
Malignant: Differentiated (papillary and follicular, Hurtle cell), poorly differentiated (island) and undifferentiated (anaplastic).
Parafollicular cells: medullary thyroid carcinoma.
Follicular cells: mixed medullary follicular tumor.
Nonepithelial "primary malignant lymphomas, sarcomas
Secondary tumors.: Classification
Differentiated carcinoma: papillary, follicular (Hürthle cell)
Medullary Carcinoma
Anaplastic or undifferentiated:
small cell, giant cell.
Other: lymphoma, Kaposi., Carcinosarcoma.
Thyroid adenoma
Frequency increases with age, greater among women
Single lesions, well demarcated, with capsule
Macro or microfoliculares, usually less than 4 cm
Extrathyroidal tissue compressed About 1% are hyperfunctioning and are the third leading cause of hyperthyroidism
CLASSIFICATION
Trabecular, fetal, colloid
Macroscopy:
Tumor spheroid, surrounded by connective tissue capsule
Brownish appearance, may have areas of fibrosis, hemorrhage and calcification
PAPILLARY CARCINOMA
Represents 75-80%, is presented at any age, but
mainly between the 3rd and 5th decade, Prior exposure to ionizing radiation, follicular cell origin, single or multiple lesions, usually with multi -
FOLLICULAR CARCINOMA
Represent 10-20% typically affects elderly women, in céls Source. Follicular
Pathology:
Nodules unique, fibrosis, calcifications, follicular or trabecular architecture, hematogenous metastasis, lung, bone, soft tissue, brain, liver
MEDULLARY CARCINOMA
Represents 5%, neuroendocrine neoplasms arising from parafollicular cells or C cells of thyroid secretes calcitonin, single or multiple lesions.
Pathology:
Polygonal cells, spindle group, deposits of amyloid.
C cell hyperplasia
MEDULLARY CARCINOMA
2 varieties:
1. Sporadic medullary cancer: 75%, unilateral and focal
2. Hereditary medullary cancer: 25%, bilateral, multicentric
Hereditary:
Autosomal dominant mutation RET proto-oncogene
MEN IIa: ca. medullary thyroid, pheochromocytoma, parathyroid hyperplasia 1st
MEN IIb: ca. medullary thyroid, pheochromocytoma, mucosal neuromas, intestinal ganglioneuroma habit marfanoid
FNA: diagnosis suggestive
Lymphatic metastases in 60 - 75%? resection Qx
10-year survival of 65%
Anaplastic or undifferentiated
Undifferentiated tumors of the thyroid follicular epithelium, represent only 1 to 2%, was present in> 65 years.
Clinical:
Dyspnea, dysphagia, dysphonia, cough.
Pathology
Cell anaplastic (pleomorphic, anaplastic spindle and small).
Px is the worst:
Survival of 7% at 5 years, early invasion adjacent structures, usually unresectable, No treatment

SUSPECTED MALIGNANT DISEASE
Young patient, male gender, family history of ca. Medullary, cervical irradiation history, firm nodule, immobile,> 2 cm, tracheal deviation, lymphadenopathy (+)
DIAGNOSIS
Clinic
Lab:
TSH, T3, T4 and free T4: functional status, TSH measurement: frenación axis by exogenous supply
Tumor markers (recurrence): Ca differentiated thyroglobulin, Ca core: calcitonin
DIAGNOSIS
FNA
For cytologic
S: 83%, E: 92%
Operator dependent, a pathologist trained at least 6 samples, looking rojizoamarillentas and immediate fixation.
FNA:
Results: Ca
Positive 97%, negative 8%, Suspicious 42%, dg not helpful for 26% (repeat sample)
Ca diagnosed papillary and medullary, but not follicular (adenomas)
DIAGNOSIS
ECO cervical most useful test, detects lesions 2-3mm
S: 86.5% and E: 92.3% (ca. not follicular)
S: 18.2% and E: 88.7% (ca. follicular)
Signs of malignancy: solid or solid-cystic, ill-defined Hypoechoic
ECO 2D vascularized in the thickness
Punctures Guide
DIAGNOSIS
Core Biopsy: Tissue, more accurate diagnosis, risk of injury (guide x ECO)
Thyroid scintigraphy: technetium or yodo131, functional studies, classifies cold, hot and warm (relative to gland: ca 15-30% Cold, Warm 9% Heat 4%), evaluates the presence of residual tissue and metastases
CT and MRI: Dissemination local, regional and remote
TREATMENT
It depends on the stage of disease, surgery, radiotherapy, chemotherapy, palliative TTO
MONITORING
Control every 6 months for 2 years, then annual
Lab: Calcitonin, thyroglobulin
Images: Rx Torazo
Study recurrence: scintigraphy, CT, MRI

DIABETES MELLITUS
Chronic hyperglycemia is associated with long-term development of macrovascular complications, microvascular and neuropathic.
Affecting large numbers of people, with a progressive increase in the prevalence of DM 1 and DM 2 explosive, the latter as
WHO links with:
The growth and aging of Lapoblación, increased obesity, wrong habits of diet, sedentary lifestyles, so it is with the emerging DM 2 associated with obesity in children
EPIDEMIOLOGY
DM affects approx. 10% of Chileans aged over 20 years of age.
Therefore, there are almost 1 million diabetics in India
DM1: 20,000
DM2: 975,000
Other: 5,000
CLASSIFICATION
Diabetes mellitus type 1: Autoimmune, Dg in childhood and adolescence, Destruction of the endocrine pancreas function
Type 2 Diabetes Mellitus: Insulin resistance, Hereditary
Gestational Diabetes
PATHOGENESIS. TYPE 2 DM
Pathophysiology
Phenomenon of Insulin Resistance, Present at the> majority of the DM2
Usually precedes the development of the state of glucose intolerance
Early stage: Compensated with insulin hypersecretion
Hyperglycemia occurs only when there is a relative insulin hyposecretion glucose
Pathophysiology
1) Genetics: hereditary disease; 35-50% deals. have relatives with diabetes
2) Impaired insulin secretion
3) Insulin resistance: alterations in the insulin receptor and
post-receptor defects, Hyperglycemia (3 mec.)
4) Inability to beta cell adaptation to the IR
5) Environmental factors in DM2: Obesity, age (? Glucose Tolerance with Age 2 °? Muscle tissue: adipose tissue), Stress, glucotoxicity (Effects of Chronic Hyperglycemia), lipotoxicity
NATURAL HISTORY OF DM
1 year IR: Pancreas off? Insulin secretion? Remain fasting and postprandial blood glucose
Then, before the manifestation of DM2:? secretory capacity of the cels. B. ®? Glucose Intolerance in range
+ IR remains? progressive levels of glycemia (2nd glucotoxicity) +? insulin secretion
Diabetes Clinic
CLINICAL
In general very little symptomatic; consultation porcomplicaciones of DM or associated pathologies, 50% dg. with laboratory tests
Classic symptoms:
polydipsia, polyuria, polyphagia, fatigue, weakness, muscle cramps ext. Lower (ppal. night), drowsiness, irritability and mood swings, acute complications, chronic microangiopathic complications and macroangiopathic
DIAGNOSIS
1. In symptomatic patients:
symptoms 2 ° to osmotic diuresis +
hyperglycemia
2. In asymptomatic patients: elevated fasting glycemia
3. In asymptomatic high risk: normal fasting blood glucose, abnormal tolerance test
CLASSIFICATION ADA 1997
Classic symptoms with casual plasma glucose? 200 mg / dl (Casual = any time of day regardless of fasting) either.
Fasting Plasma Glucose? 126 mg / dl (fasting = 8 or more hours without
intake) on two occasions
Glucose in plasma at 2 hours a TTGO? 200 mg / dl (glucosadebe load be 75 ml.)
Fasting glycemia CATEGORIES
70-99 mg / dl = normal
100 to 125 mg / dl = impaired fasting glycaemia
? 126 mg / dl = provisional diagnosis of Diabetes Mellitus
Glucose intolerance
Is a disease state (higher morbidity
and risk of DM)
Glycemia at 2 hours post load with 75 grams of glucose between 140 and 199 mg / dl
The diagnosis is not based on fasting blood glucose levels because it underestimates by 30%
Therefore, with impaired fasting glucose (100 to 125 mg / dl): TTGO request a 75-gram.
Oral hypoglycemic AMBULATORY TYPE 2 IN D
only for type 2 diabetes, not type 1 diabetes, not pregnant
three main groups:
sulfonylureas
(insulinosecretoras): normal weight or slightly weaker
alternatively: meglitinides
biguanides (insulin sensitizer): overweight-obese
known since 1930
Thiazolidinediones (insulin sensitizer)
SULFONYLUREAS
Tolbutamide: (1956), is rapidly degraded in the liver ® ® inactive metabolite renal excretion in 24 hr
half-life 6.8 hrs, use with caution in patients with impaired renal function, useful in elderly diabetics.
Chlorpropamide: it is the most active, slow and partial liver metabolism ® active metabolite, 60% renal excretion
half-life from 36 to 72 hours, risk of hypoglycemia (fallarenal contraindicated in patients or edadavanzada)
Induces water retention and hyponatremia porestímulo ADH (useful endiabetes insipidus)
Glibencamida: Single crossing the mb of CEL. Beta (+ insulin synthesis)
Average life: 10 hrs, Peak action at 4 pm, rapid metabolism
Liver, 50% and 50% renal impairment.
Glimepiride: rapid absorption, peak action at 2 - 3hrs
Average life: 10 hrs, renal elimination (metabolites inactive) 60%
and biliary 40%, Administration 1 time days
Adverse Reactions: Low frequency (1 to 5%), cause the withdrawal tto
GI intolerance: exceptional, nausea, vomiting, diarrhea
Skin reactions: rash dermatitisexfoliativa fotosensibilidadpúrpuray-Stevenjohnson Sd.
Alt. Hemic: Infrequent agranulocytosis, thrombocytopenia, pancytopenia, anemia, hemolytic, and eosinophilia.
Liver disorders: mechanism idiosyncratic cholestatic jaundice
transient.
Hypoglycemia: more frequent and Glibencamida Chlorpropamide

BIGUANIDE-2
METFORMIN:? TG and LDL: HDL, Mild anorectic effect
DIRECTIONS:
reduction of fasting blood glucose rather than postprandial, monotherapy in obese, prevention of T2DM in obese laglucosa intolerant.
Dose: 500-1700 mg daily
PRECAUCIÓNCONTRAINDICACIÓN:
dye (48 HRS before Suepender)
kidney damage: albuminuria,
creatinine> 1.4 mg / dl
heart failure, liver infection
SIDE EFFECTS: Diarrhea, lactic acidosis, dialysis immediately
yet: mortality 50%
ACUTE COMPLICATIONS OF DIABETES
Diabetic ketoacidosis: Incidence? 4 to 12 epis/1000
pctes / year, Debut 25 to 40% DM 1
Mortality: 3.3% (1911-1920 40%), 70% vascular (mesenteric thrombosis,
BIRD, MI), 5% infection (septic shock)
CAUSES
Abandonment use insulin or HGO, insulin administration errors, control, DM Debut T1 (children), Infections
Drugs: GCC, lithium, Tz, OH intox, cocaine, Stress Psiq.
Vascular: AVE, IAM
Multiple trauma, acute pancreatitis
PATHOPHYSIOLOGY
Insulin bid ® 0 v / s demand?
Hm excess counterregulation: GGCC ® Glucagon + + +
I nsulina 0 + exchange activity hyperglycemia ® E hepatic
+ ® is not Glucagon ® pyruvate gluconeogenesis glycolysis ®
Glucagon + + catecolam ins 0 ® glycogenolysis
In 0 ®? GLUT 4 ® <<<<collection
Hiperglic +? catechol and lipolysis HCrec ® ®? AGL pl
N: or VLDL pass TRG
CAD: carnitine CCetónicos ® ® ® HCO3 keto? 0 = AG metabolic acidosis?
CLINICAL
Symptoms: Nausea / vomiting, thirst / polyuria, abd pain, dyspnea
Signs:? FC, dry mucous / low turgor, dehydration / mortgage, Kussmaul / constraint respiratory Abd acute fever, impaired consciousness
1 .- preferred management option in ICU
Priorities:
1. Replacement fluids
2. Insulin
3. Replenishment of K
Administer bicarbonate, phosphate, magnesium is not 1st line
2 REPLACEMENT FLUIDS
a) To replace blood volume
Recent weight - current weight, Hipot º A? (-) 10% blood volume, 0.9% SF, 1L fast, continue 1 L / h
b) Replace the body of water deficit
SF 0.45% 150 to 500 cc / h, according fx card / kidney / dehydration, Monitor go? contribution? obj BH (+) 6L
3 INSULIN THERAPY
Obj ® (-) ketogenesis and <hyperglycemia
a) regular insulin 10 to 15 U bolus EV
b) BIC insulin 5 to 10 U / h or 0.1 U / kg / h: 100 U InRg / 500 cc ® 50 cc / h ® 10 U / h
Lowering blood glucose: Appropriate ® 50 to 70 mg / dl / h, Stamina ®? 50 to 100% dose times, excessively rapid ® encephalopathy osmotic
4 K
Obj ® K in rank n, pl levels and ECG at baseline, giving 10 to 20 mEq / h of routine, except K> 6 / alt ECG / IRA, oliguria, If hypokalemia ® 40 mEq / h, Adm KCl, ® pass phosphate K.
5 CONTROL
Na? x? glycemia, but ® hydration free water
Anion Gap ® metabolic recovery
Monitor weight, BH, consciousness level.
COMPLICATIONS CAD
1. Lactic acidosis
2. Arterial thrombosis
3. Cerebral edema
- Poor prognosis,> In children, hypertension º IC ® obs if: headache, papilledema,? Alertness.
FR: hydration / rapid correction
Dg TAC
TTO ® Dg fast EV + Mannitol can prevent damage if he survives.
Nonketotic hyperosmolar state
T2 DM, advanced age, severe dehydration, hyperglycemia ++++, leg, absence of acidosis, OPA> 300, OPT> 340, rising incidence, mortality 15% (previously 60%)
Etiology: Infection 50%
CLINICAL
Insidious, hyperosmolar decompensation previous stage of deterioration increased alert + + ® coma neurological symptoms,
50% pactes.
Advanced age, impaired thirst center ® aggravates dehydration.

1. Fluid replacement
2. Insulin therapy
3. Correction ELP deficit
EV Access and support measures, Precipitating factors
HYPOGLYCEMIA
Whipple's triad, Brain ® ® does not synthesize glucose intake
continuous.
Stabilization glycemia: Diet / Fasting (glycogen) 8 - 12h (<) /
gluconeogenesis
Fasting Insulin = low
Hypoglycemias ® CGCG levels, thresholds
CLINICAL
Neuroglycopenic: Altcomportamiento, Confusion, Weakness, convulsions, unconsciousness, coma,
death (severe yprol)
Autonomous: Adrenergic, palpitations, tremor, anxiety, Cholinergic, diaphoresis, hunger, paresthesias
CONVENTIONAL RISK FACTORS
EXCESS INSULIN OR HGO, Mala dosing reduces glucose intake (night),> use glucose (exercise),> sensitivity to glucose (? Weight, tto), <endogenous glucose production (pos
OH), <glucose clearance (IRC)


AUTONOMIC FAILURE
Decreased counterregulatory hormonal response, altering glucose production
Unexpected Hypoglycemia: 1 sint neuroglycopenic, hipoglic It involves serious
1 HDC easily absorbed
VO pactes conscious must always be easily accessible
2 ampoules SG 30%
Severe hypoglycemia, altered consciousness
Initial bolus 20 to 50 cc SG 50%? 25g IV
SG infusion to maintain 10% HGT> 100mg/dl
3 Glucagon
1 mg IM or SC,
Tto effective ® initial impairment of consciousness or if there is access EV
Vomiting ® RAM ® airway protection
Family education, availability Kit
4 education
Talking ® causes - prevention - appropriate dose adjustments - diet --
scheme exercises, etc..
Tto DM intensive, may not recognize hypoglycemia ® HGT freq
and measures for its correction
Nonselective beta-blockers Contrindicados

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