Renal Diseases

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Renal Diseases

• AH 120

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The Nephron The Functional Unit of the Kidney
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HypertensionSystolic BP gt 140 mmhg and/or
Diastolic BP gt 90 mmhg

• Mechanism is similar to what happens in CHF
• Decreased pressure sensed by JG cells activates
  the renin-angiotensin-aldosterone mechanism
• Atherosclerosis is the probable cause of the J-G
  cells not sensing proper pressure in renal blood
  flow
• Treated by diet, exercise, and drugs
• ACE inhibitors, Calcium channel blockers, Beta
  blockers, diuretics

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Pyelonephritis

• Inflammation of the renal pelvis and interstitial
  tissue of the kidney

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Etiology

• Bacterial infection that often spreads retrograde
  from the bladder (cystitis)
• Common agents E-Coli, Strep, and Staph

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Pathology

• Intense inflammation causes abscesses to from in
  renal pelvis and interstitial tissue
• If severe enough, the kidneys may fail
• Can be acute or chronic
• Fibrosis will be present if chronic

Acute
Chronic
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Signs Symptoms

• Fever
• Flank Pain
• U.A. shows pyuria and bacteriuria
• Urinary signs frequency, urgency, and burning

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Treatment

• Antibiotics
• If severe enough to cause renal failure, then
  renal dialysis is indicated

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Glomerulonephritis

• Inflammation of the glomerulus caused by a
  reaction to immune complexes and complement
• It can be acute or chronic

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Etiology

• Usually caused by a strep infection
• Strep throat
• Strep skin lesion

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Pathology

• Immune complexes and compliment damage glomerular
  membrane and cause it to become more permeable
• WBCs, RBCs , and plasma proteins pass into
  Bowmans capsule

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Signs Symptoms

• Initial strep infection
• Urinary signs
• Hematuria, proteinuria, dark urine, decreased
  output
• Facial and ankle edema
• Due to hypoproteinemia and sodium and fluid
  retention
• Hypertension
• Possible renal failure

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Treatment

• Supportive treatment if acute
• If chronic, patient may eventually need dialysis
  and/or transplant

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Renal Failure

• Failure of the kidney to adequately remove waste
  products and maintain fluid and electrolytes.
• It can be an acute or chronic process

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Etiology

• Damage due to disease processes, e.g.,
  pyelonephritis , glomerulonephritis, etc
• Reduced renal blood flow (shock)
• Burns, trauma, dehydration
• Toxins
• CCL4, Hg, ethylene glycol

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Signs Symptoms

• Lab Findings
• Decreased urine output
• Increased BUN, uric acid, creatinine, and ammonia
• Decreased pH
• Abnormal electrolyte levels
• Anemia (if chronic) due to decreased
  erythropoietin

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Treatment
Hemodialysis (for acute or chronic failure)
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Treatment (cont.)
Transplant
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Pulmonary Diseases

• May involve the airways and/or the alveoli

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Pulmonary Disease Is Classified By the Effect on
Pulmonary Function
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Restrictive Pulmonary Disease

• Decreased volumes during PFT
• Lesion is in the alveolar portion of the lung or
  the chest wall
• Primarily occurs during inspiration

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Obstructive Pulmonary Disease

• Decreased flow rates during PFT
• Lesion is usually in the airways
• Primarily occurs during exhalation

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Obstructive Diseases Caused By Airway Inflammation
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Airway Inflammation Causes Obstruction because of
the following three things

• Mucosal edema
• Bronchospasm
• Increased production of thick mucus
• These three things encroach on the airway lumen
  making it harder for air to flow through the
  airways
• Harder to get oxygen in and harder to get carbon
  dioxide out

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Airway Inflammation Treatment

• Re-establish airway patency
• Drugs to reduce mucosal edema and bronchospasm
• Oral or systemic hydration to keep viscosity of
  mucus normal
• Oxygen PRN
• Mechanical ventilation PRN

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Examples of Airway Inflammatory Diseases
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The Common Cold

• Usually viral in origin

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Croup and Epiglottitis

• Croup
• Usually affects very young and is a result of a
  viral infection
• Involves larynx, trachea, and both main stem
  bronchi and develops rapidly
• Epiglottitis
• Affects mostly older children and is caused by
  H.Flu

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Acute Bronchitis(Chest Cold)

• Inflammation in the trachea, main stem and
  segmental bronchi
• Usually a complication of a viral infection

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Asthma

• Transient inflammation of the airways

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ETIOLOGY(Triggers)

• Allergy
• Infection
• Stress/emotion
• Noxious fumes
• Cold air
• Exercise

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Pathology

• Trigger mechanism causes mast cells on airways
  to degranulate and release histamine
• Mast cells often degranulate if IgE antibody and
  antigen (allergen) attach to it or if
  parasympathetic stimulation exceeds sympathetic
  stimulation
• Histamine causes inflammatory reaction in airways
• Mucosal edema, bronchospasm, increased production
  of thick mucus

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Signs and Symptoms

• During attack
• Respiratory distress
• Dyspnea
• Tachypnea
• Wheezing
• Cough (may or may not be productive)
• Cyanosis in severe attack

In between attacks, patients are relatively
symptom free!
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Treatment(During Attack)

• Inhaled drugs that stimulate the sympathetic
  nervous system
• Relieves bronchospasm
• May also be given systemically
• Albuterol (Proventil) and other similar drugs
• If hospitalization required
• Oxygen therapy possibly mechanical ventilation
• Systemic steroids (for anti-inflammatory effect)

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Prevention

• Avoidance of triggers
• Inhaled steroids
• Budesonide, fluticasone
• NSAIDS
• Cromolyn sodium, nedocromil sodium,
• Zafirlukast, montelukast
• Immuno-therapy

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Chronic Bronchitis

• Productive cough for at least three months of the
  year during a two year period

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Etiology

• Chronic Irritation
• Cigarette smoking
• Pollution
• Noxious fumes
• Chronic/recurrent infection

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Pathology

• Metaplastic change ciliated, columnar epithelium
  becomes squamous and non-ciliated
• Hyperplasia/hypertrophy of goblet cells
• Weakened, fibrotic airways that collapse easily

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Emphysema

• Hyperinflation of alveoli with destruction of
  alveolar septa, pulmonary capillary bed, and
  elastic tissue in alveolar wall

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Etiology

• Cigarette smoking
• Alpha-1 anti-trypsin deficiency
• Usually a genetic defect

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Pathology

• Proteolytic enzymes are activated in the lung due
  to either substance found in cigarette smoke or
  due to lack of alpha-1 anti-trypsin
• Proteolytic enzymes cause
• Destruction of alveolar septa
• Destruction of pulmonary capillary bed
• Destruction of elastic tissue in alveolar walls

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Result is many alveoli coalesce to form large,
hyperinflated alveoli that inflate easily but do
not return to their normal volume during
exhalation. Because of destruction of the
pulmonary capillary bed, there is less surface
area for gas exchange.
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Normal
Emphysema
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Chest X-Ray
Barrel chest
Increased retro-sternal airspace
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COPD Chronic Obstructive Pulmonary DiseaseA
mixture of emphysema and chronic bronchitis
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Emphysema Dominant Pink Puffer

• Works hard enough to maintain acceptable levels
  of O2 and CO2
• Good color
• Appears S.O.B most of time
• Minimal sputum
• Emaciated appearance
• Heart failure occurs late

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Chronic Bronchitis Dominant Blue Bloater

• Does not work as hard so has poor color and does
  not appear to be as S.O.B. as the pink puffer
• Lots of sputum production
• Minimal weight loss
• Heart failure occurs early

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COPD Complication Cor Pulmonale

• Heart failure due to lung disease

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• Due to hyperinflated alveoli compressing
  pulmonary capillaries and there not being as many
  capillaries, pulmonary hypertension develops
• This increases the work on the right heart which
  eventually hypertrophies and then starts to fail

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Cor Pulmonale Signs Symptoms

• Enlarged right heart
• Jugular Venous Distension (JVD)
• Ankle edema
• Arrhythmias
• Usually atrial
• Prone to pulmonary infections

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Maintain Oxygenation(this may require continuous
O2)
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Other Treatment Options

• Lung transplant
• LVRS (Lung Volume Reduction Surgery)
• Resect the most damaged part of the lung(s)

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Restrictive Pulmonary Disease

• Decreased volumes during PFT
• Lesion is in the alveolar portion of the lung or
  the chest wall
• Primarily occurs during inspiration

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Pneumoconiosis

• Lung disease caused by inhalation of dust
  particles

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Etiology

• Often due to occupational exposure
• Silicosis
• Coal Workers Pneumoconiosis
• Asbestosis

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Pathology

• Prolonged inhalation of dust particles causing
  chronic inflammatory response in the alveoli
• Results in fibrosis (scar tissue)

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Manifestations

• CXR shows interstitial fibrosis
• Dyspnea on exertion that progresses to dyspnea at
  rest
• Hypoxia
• PFTs show restriction
• Lung biopsy shows presence of dust particles

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Treatment

• Prevention is best
• Symptoms may take 10-20 years of exposure before
  they develop
• Oxygen therapy
• Lung transplant

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ARDS(Acute Respiratory Distress Syndrome)

• Also known as shock lung, acute lung injury
  (ALI), post-traumatic pulmonary insufficiency

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Etiology

• Inhalation insults
• Noxious gases, aspiration of gastric contents
• Circulatory insults
• Shock from trauma/hemorrhage, sepsis

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Pathology

• Insult triggers vasoactive substances that
  damage the alveolar-capillary membrane
• Damage allows protein rich fluid to leak into
  interstitial spaces and alveoli
• Non-cardiogenic pulmonary edema
• Also inhibits alveolar type II cells ability to
  produce surfactant
• Leads to progressive atelectasis

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Manifestations

• Progressive dyspnea and S.O.B.
• Progressive hypoxia
• Gas exchange may be so impaired to cause death
• CXR initially lags symptoms by about 24 hours
• Patient may have dry, non-productive cough

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Treatment

• Support oxygenation and ventilation
• May require aggressive mechanical ventilation
• Even with aggressive treatment, mortality is
  still around 50-60

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Pneumonia

• Inflammation of the lung at the alveolar level

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Etiology

• Infection
• Aspiration

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Pathology Stage 1 Inflammation
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Pathology Stage 2 Consolidation
Alveoli are now filled with inflammatory
exudate. Inflammation may spread to pleura
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Pathology Stage 3Resolution

• Exudate in alveoli starts to break up
• Patient starts coughing productively to clear the
  exudate and re-aerate the lung

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Manifestations

• Fever Chills
• Dyspnea and S.O.B.
• Hypoxia
• Pleuritic chest pain
• Abnormal breath sounds
• Cough (only becomes productive during resolution
  phase)

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Treatment

• Drug therapy for infection
• Fluids (P.O. or IV)
• Oxygen for hypoxia
• Respiratory care to get to resolution phase

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Pulmonary Edema

• Leakage of fluid from pulmonary capillaries
  causing the fluid to accumulate in the
  interstitium and then to spill into the alveoli

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Pulmonary Hemodynamics
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Etiology

• Increased hydrostatic pressure
• CHF, fluid overload
• Decreased osmotic pressure
• Loss of plasma proteins (albumin) due to blood,
  loss, liver disease, kidney disease
• Altered capillary permeability
• Neurogenic , eg, head trauma, heroin OD, triggers
  of ARDS

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Pathology

• Fluid accumulates in interstitium and alveoli
• Leads to restriction and atelectasis and poor gas
  exchange

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Manifestations

• Dyspnea and S.O.B
• crackles breath sounds indicating alveoli and
  small airway collapse
• If severe enough, audible gurgling sounds will be
  heard
• Hypoxia
• Patient may cough up pink, frothy fluid

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Treatment

• For increased hydrostatic pressure diuretics, eg
  Lasix
• For decreased osmotic pressure whole blood or
  albumin
• For altered capillary permeability support
  oxygenation and ventilation until condition
  stabilizes
• May require mechanical ventilation

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Pulmonary Diseases That May Cause Restriction,
Obstruction, or Both

• Lesions may occur in airways and/or alveoli

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Tuberculosis

• An infectious disease that usually starts in the
  lung and spreads throughout the body

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Etiology Mycobacterium Tuberculosis
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Pathology

• Initially forms a tubercle
• Bacillus is surrounded by WBCs
• This initial, primary lesion is called a Ghon
  lesion
• If immune system wins, tubercle is controlled
  and eventually becomes calcified

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Pathology (cont.)

• If immune system is overwhelmed, Tb bacillus
  starts consuming lung tissue causing caseous
  lesions
• May now spread to other body organs

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Manifestations

• No symptoms with initial infection
• If bacillus starts to spread and consume lung
• Weight loss
• Fatigue
• Tachycardia
• Night sweats
• Hemoptysis
• Hypoxia
• Note these symptoms are very similar to lung
  cancer

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Diagnostic Tests

• Skin test
• CXR look for either calcified lesions or
  caseous lesions
• Sputum Cytology
• Gram stain and AFB

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Treatment

• Is step therapy
• Step I (for prophylaxis in high risk patients
  with positive skin test) - INH
• Step II (for active disease) INH plus rifampin,
  ethambutol, or pyrazinamide (one of these three)
• Step III (for severe active disease) Steps I
  and II plus streptomycin

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Coccidioidomycosis

• Fungal disease caused by coccidioides immitis
• Is endemic in soil of the southwest
• Etiology fungus is inhaled when dust from soil
  is spread by wind
• Pathology similar to Tb. Either calcified or
  caseating lesions and may spread to other organs

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Coccidioidomycosis (cont.)

• Manifestations
• Fever, fatigue, achy muscles and joints
• Pleuritic chest pain
• Dry, non-productive cough
• Diagnostic tests sputum cytology and skin test
• Treatment antifungal drugs, eg amphotericin B

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Lung Cancer

• Bronchogenic Carcinoma

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Squamous Cell Carcinoma

• Tumors develop in the large, central airways
• Most common lung cancer seen in smokers

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Adenocarcinoma

• Tumor arises from glandular cells in peripheral
  airways

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Pathology

• Tumors spread not only through the lung but
  metastasize easily and early because of vascular
  and lymphatic access
• Metastasis may occur before any symptoms develop

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Manifestations

• None initially
• Dyspnea/S.O.B on exertion that progresses to
  dyspnea/S.O.B. at rest
• Fatigue and unexplained weight loss
• Dry, persistent cough that may progress to
  hemoptysis

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Diagnostic Tests

• CXR, CT Scan, MRI
• Sputum cytology
• Biopsy
• May be needle biopsy or done by bronchoscopy

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Treatment

• Surgery if the tumor has not metastasized
• Surgery may be done palliatively if metastasis
  has occurred
• Palliative resection may also be done by laser
• Chemo- and radiation therapy

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Pulmonary Embolism

• A blood clot or fatty tissue that has become free
  within the blood and then gets trapped in the
  pulmonary circulation

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Etiology

• Atherosclerotic coronary arteries
• Deep veins of the legs
• Deep Venous Thrombosis
• Fatty tissue from the marrow of long bones when
  fracture occurs

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Etiology Predisposing Factors
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Manifestations(Sudden Onset)

• Severity of symptoms depends on size and location
• Dyspnea/S.O.B.
• May or may not have chest pain
• Normal temperature or slight elevation

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Diagnostic Tests

• Lung Scan compares distribution of ventilation
  to perfusion
• Pulmonary angiogram

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Prevention is best! Thrombolytic drugs may be
used for both treatment and prevention
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Respiratory Failure

• Any disease process (or injury) that interferes
  with gas exchange
• Oxygen levels drop and carbon dioxide levels
  start to rise

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Treatment Mechanical Ventilation
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Endocrine Diseases

• AH 120

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The Pituitary, The Master Gland

• Anterior part secretes growth hormone
  (somatatropin) as well as stimulating hormones
  for other glands.
• Posterior part secretes oxytocin and antidiuretic
  hormone)

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Hyperpituitarism

• Excess growth hormone usually because of benign
  tumor
• If before puberty, excessive growth in long
  bones, hands, feet, and head (pituitary giant)
• Decreased mental and sexual development

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Acromegaly(Hyperpituitarism AFTER puberty)

• Hands, feet, and face enlarge (especially lower
  jaw)
• Coarse facial features with thickened tongue and
  curvature of the spine

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Treatment

• Resect tumor (if accessible)
• And/or radiation to shrink tumor

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Hypopituitarism

• Decreased or absent production of anterior
  pituitary hormones
• Etiology head injury, ischemic damage, possibly
  tumor
• Results in decreased growth hormone and decreased
  stimulating hormones for the other glands
• Other glands will malfunction

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Pituitary Dwarf (hyposecretion BEFORE puberty)

• Small but usually proportional
• Other glands dysfunction, eg does not go through
  puberty
• Usually very mentally sharp
• Responds to hormonal replacement
• Growth hormone needs to be administered before
  ends of long bones seal

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Simmonds Syndrome(Chronic adult hypopituitarism)

• Causes premature aging and senility
• Weak, dry and wrinkled skin
• Loss of pubic and axillary air
• Sex organ atrophy
• Loss of drive and interest
• May respond to hormonal supplement if diagnosed!

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Diabetes Insipidus(Decreased secretion of ADH)

• Etiology heredity, trauma or disease that
  damages posterior pituitary
• Pathology excess water loss through kidneys
  because of insufficient ADH
• May lead to dehydration and shock
• Signs Symptoms Polydipsia and Polyuria,
  weakness/fatigue
• Treatment Administration of ADH

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Thyroid Gland

• Secretes thyroxin which regulates metabolic rate

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Hyperthyroidism

• Also known as Graves Disease
• Gland hypertrophies and produces too much
  thyroxin
• Etiology
• Benign or cancerous tumors
• Idiopathic

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Signs Symptoms
And, exopthalmos
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Treatment

• Medication to inhibit thyroxin and/or its
  secretion
• Surgery and/or radiation for neoplasms on thyroid
• Surgery and/or radiation could cause the patient
  to develop HYPOTHYROIDISM

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Hypothyroidism

• Also known as Myxedema
• Etiology
• Damage from disease, surgery or radiation
• Hypopituitarism
• Autoimmune reaction
• Pathology decreased thyroxin causes decrease in
  metabolic rate

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Signs Symptoms
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Neonatal Hypothyroidism

• Also know as Cretinism
• Etiology congenital malformation of the thyroid
  or genetic defect that interferes with thyroxin
  production
• Pathology Low thyroxin inhibits mental and
  physical development

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Treatment

• Blood test to determine presence
• Administration of thyroxin
• If not diagnosed and treated, there is permanent
  impaired mental and physical development

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Non-toxic Goiter

• Enlargement of thyroid without affecting function
• May interfere with swallowing and breathing!
• Etiology iodine deficiency, enzyme deficiency,
  increased hormone requirement
• Treatment Medicationssometimes surgery

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Adrenal Glands

• Cortex secretes mineral corticoids
  glucocorticoids and sex hormones.
• Medulla secretes norepinephrine and epinephrine

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Hyperadrenalism

• Also known as Cushings Syndrome
• Excess levels of glucocorticoids which alters
  metabolism of proteins, glucose(carbohydrate),
  and lipids (fat)
• Etiology Benign or cancerous tumor on adrenal or
  pituitary, exogenous administration of steroids

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Signs Symptoms

• Hyperglycemia
• Lipid mobilization
• Truncal obesity with thin limbs, moon face, fat
  pad between shoulders (Buffalo hump)
• Hypertension due to sodium and fluid retention
• Muscle weakness due to potassium loss
• Striae and bruises
• Poorly healing wounds tendency to get infections
• Mood swings

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Treatment

• If due to tumor, surgery to resect it
• Taper steroid drug use
• Prolonged steroid use may allow gland to atrophy
  due to decreased ACTH

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Hypoadrenalism

• Also known as Addisons Disease
• Decreased glucocorticoids and mineral corticoids
• Etiology
• Autoimmune reaction that damages the gland
• Atrophy from steroid drug administration/abuse

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Signs and Symptoms

• Low aldosterone causes fluid and sodium loss with
  potassium retention
• Low blood pressure and weakness and fatigue
• Weight loss with G.I. disturbances
• Areas of excess pigmentation and/or absent
  pigmentation

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Pheochromocytoma

• A benign tumor on the adrenal medulla that causes
  transient, excess release of norepinephrine and
  epinephrine
• Causes sudden rise in blood pressure and cardiac
  output
• May lead to heart attack or CVA (stroke)
• If diagnosed, treatment is surgical removal of
  tumor

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Parathyroid Glands

• Secrete parathormone which regulates blood levels
  of calcium

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Hyperparathyroidism

• Increased parathormone levels
• Usually due to benign adenoma
• Causes calcium levels to rise in blood by
  allowing it to come out of bone
• Manifestations muscle weakness, weak bones that
  are painful and fracture easily, kidney stones
• Treatment surgical removal of tumor

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Hypoparathyroidism

• Low parathormone levels
• Caused by surgical/radiation damage to thyroid
  that affects parathyroid autoimmune reaction
  that damages gland
• Manifestations low calcium blood levels, muscle
  tetany and hyperexcitable nervous system
• Treated by increasing calcium and vitamin D in
  diet

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SAMPLE TEST QUESTIONS!
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Over production of parathyroid hormone produces
which of these

• II only
• I and III
• I and IV
• II and III
• II and IV

• Tetany
• Muscle weakness
• Increased blood levels of calcium
• Decreased blood levels of calcium

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Permanent destruction of alveolar tissue leading
to loss of elastic recoil, over-inflation of
alveoli, and loss of alveolar septa best
describes

• COPD
• Asthma
• Emphysema
• Chronic bronchitis
• Pneumonia

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A bacterial infection in the renal pelvis and
interstitial tissue best describes

• Glomerulonephritis
• Uremia
• Pyelonephritis
• Cystadenoma
• Renal tubular necrosis

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Airway changes that occur with chronic bronchitis
include

• I and IV
• II and III
• I, II and III
• II, III, and IV
• I, II, III, and IV

• Weak airways that tend to collapse during
  exhalation
• Mucus gland hypertrophy
• Loss of cilia
• Squamous metaplasia of the epithelium

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Enlargement of the thyroid that does not
necessarily affect its function best defines

• Goiter
• Throma
• Pheochromocytoma
• Endoma
• Outoma

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A patient receiving INH (Isoniazid) is probably
be treating for which lung disease?

• Pneumonia
• Coccidioidomycosis
• Bronchogenic carcinoma
• Tuberculosis
• Asthma

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What abnormality of pulmonary function occurs
with obstructive pulmonary disease?

• Reduced lung volumes
• Reduced flow rate of gas during exhalation
• Increased lung volumes
• Increased flow rate of gas during exhalation
• Inability to perform a breath holding maneuver

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When renal function ceases, the appropriate
treatment is

• Hemodialysis
• Blood transfusion
• Renal resection
• Drug therapy
• Purchase of additional life insurance