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PATHOPHYSIOLOG

Y OF COPD
(WITH SPECIFIC ASSESSMENT FOCUS & MANAGEMENT)
Bhon Lhester B. Valendez
DEFINITION OF TERMS.
PATHOPHYSIOLOGY (NARRATIVE)

airfow limitation is both progressive and


associated with an abnormal infammatory
response of the lungs to noxious particles or
gases.

Because of the chronic infammation and the


bodys attempts to repair it. narrowing occurs in
the small peripheral airways.

Over time, injury-and-repair process may occur.

Airfow obstruction may also be due to


parenchymal destruction as seen with
emphysema, a disease of the alveoli or gas
exchange units.
EMPHYSEMA

impaired gas exchange (oxygen, carbon dioxide)


results from destruction of the walls of over
distended alveoli.

a pathological term that describes an abnormal


distention of the air spaces beyond the terminal
bronchioles, with destruction of the walls of the
alveoli.

As the alveolar walls continue to break down, the


pulmonary capillary bed is reduced.
2 major changes in pulmonary Emphysema:

Loss of lung elasticity.

Hyperinfation of the lungs.


2 Classifcation of Emphysema:

Panlobular

Centrilobular
CHRONIC BRONCHITIS

Infammation of the Bronchi or Bronchus.

Caused by Irritants.

Diferent from Emphysema.


ETIOLOGY

smoking.
- most important risk factor.
- triggers production of excessive protease.
- Passive smoking
- active smoking
- exposure to occupational dusts
- chemicals, indoor air pollution,
- and outdoor air pollution.
COMPLICATIONS

Hypoxemia and acidosis

Respiratory infection (S. Pneumoniae)

Cor Pulmonale

Cardiac dysrhythmias.
Chronic
Bronchitis
Chronic
Bronchitis
Pulmonary
Emphysema
COPD
COPD
Airway
Problem
Alveolar
Problem
CLINICAL MANIFESTATION
Appearance:

Slow moving

Slightly stooped.

Sit with forward-bending position w/ arms held


forward.
Respiratory changes:

Breathes w/ rapid shallow respiration.

Use of accessory muscle (neck and abdomen).

RR as high as 40-50 cpm.

Limited diaphragmatic movement (Excursion)

Decrease vibration (Fremitus)

Crackles

Cyanosis

Delayed capillary refll

Clubbing of the fngers. (Dec. arterial O2 levels).


Cardiac changes:

Swelling of feet and ankles ( Cor Pulmonale).


Laboratory assessments:

Hypoxemia

Hypercarbia.

Polycythemia
MANAGEMENT:
Non-surgical:

Airway maintenance:
* clients head, neck, and chest align.
* liquify secretions and clear the airway.

O2 therapy:
* 2-4 LPM via nasal cannula.

Drug therapy:
* Mucolytic
* Bronchodilators
* Corticosteroids.
Surgical:

Lung reduction surgery.


Post-operative care:

Diaphragmatic or abdominal breathing.

Pursed-lips breathing.

Positioning.
* upright position w/ bed of head elevated.

Coughing technique.

Chest physiotherapy and postural drainage.

Suctioning.

Hydration.
PATHOPHYSIOLOGY
OF DIABETES
DEFINITION OF TERMS

diabetes mellitus: a group of metabolic diseases


characterized by hyperglycemia resulting from
defects in insulin secretion, insulin action, or
both.

hyperglycemia: elevated blood glucose level


fasting level greater than 110 mg/dL (6.1
mmol/L); 2-hour postprandial level greater than
140 mg/dL (7.8 mmol/L).

hypoglycemia: low blood glucose level (less than


60 mg/dL [less than 2.7 mmol/L]).

ketone: a highly acidic substance formed when


the liver breaks down free fatty acids in the
absence of insulin. The result is diabetic
ketoacidosis.

retinopathy: a long-term complication of


diabetes in which the microvascular system of the
eye is damaged.

insulin: a hormone secreted by the beta cells of


the islets of Langerhans of the pancreas that is
necessary for the metabolism of carbohydrates,
proteins, and fats; a defciency of insulin results
in diabetes mellitus.

type 1 diabetes: a metabolic disorder


characterized by an absence of insulin production
and secretion from autoimmune destruction of
the beta cells of the islets of Langerhans in the
pancreas. Formerly called insulin-dependent,
juvenile or type I diabetes.

type 2 diabetes: a metabolic disorder


characterized by the relative defciency of insulin
production and a decreased insulin action and
increased insulin resistance. Formerly called non-
insulin-dependent, adult-onset, or type II
diabetes.
FUNCTION OF INSULIN

Insulin is secreted by beta cells, which are one of


four types of cells in the islets of Langerhans in
the pancreas.

Transports and metabolizes glucose for energy.

Stimulates storage of glucose in the liver and


muscle (in the form of glycogen).

Signals the liver to stop the release of glucose.

Enhances storage of dietary fat in adipose tissue.

Accelerates transport of amino acids (derived


from dietary ) into cells.
TYPE 1 DIABETES

characterized by destruction of the pancreatic


beta cells.

It is thought that combined genetic, immunologic,


and possibly environmental

Regardless of the specifc etiology, the destruction


of the beta cells results in decreased insulin
production, unchecked glucose production by the
liver, and fasting hyperglycemia.

In addition, glucose derived from food cannot be


stored in the liver but instead remains in the
bloodstream
TYPE 2 DIABETES

The two main problems related to insulin in type


2 diabetes are insulin resistance and impaired
insulin secretion.

Insulin resistance refers to a decreased tissue


sensitivity to insulin.

In type 2 diabetes, these intracellular reactions


are diminished, thus rendering insulin less
efective at stimulating glucose uptake.

To overcome insulin resistance and to prevent the


buildup of glucose in the blood, increased
amounts of insulin must be secreted to maintain
the glucose level at a normal or slightly elevated
level.

Type 2 diabetes occurs most commonly in people


older than 30 years who are obese, although its
incidence is increasing in younger adults.
CLINICAL MANIFESTATIONS

3 Ps
- Polyuria (increased urination)
- polydipsia (increased thirst)
- polyphagia (increased appetite).

fatigu

weakness,

sudden vision changes,

tingling or numbness in hands feet,

dry skin,

skin lesions or wounds that are slow to heal, and

recurrent infections.
ASSESSMENT AND DIAGNOSTIC
FINDINGS

Fasting plasma glucose (FPG) levels of 126


mg/dL (7.0 mmol/L) or more or random plasma
glucose levels exceeding 200 mg/dL (11.1 mmol/L)
on more than one occasion are diagnostic of
diabetes.
DIABETES MANAGEMENT

The main goal of diabetes treatment is to


normalize insulin activity and blood glucose
levels.

The major adverse efect of intensive therapy was


a threefold increase in the incidence of severe
hypoglycemia (severe enough to require
assistance from another person), coma, or
seizure.
NUTRITIONAL MANAGEMENT

Nutritional management

Exercise

Monitoring

Pharmacologic therapy

Education
COMPLICATIONS

HYPOGLYCEMIA (INSULIN REACTIONS)


Man:
- Three or four commercially prepared glucose
tablets
- 4 to 6 oz of fruit juice or regular soda
- 6 to 10 Life Savers or other hard candies
- 2 to 3 teaspoons of sugar or honey
DIABETIC KETOACIDOSIS

Hyperglycemia

Dehydration and electrolyte loss

Acidosis

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