Professional Documents
Culture Documents
AH 120
The Nephron: The Functional
Unit of the Kidney
Hypertension
Systolic BP > 140 mmhg and/or
Diastolic BP > 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
Pyelonephritis:
Chronic
Signs & Symptoms
• Fever
• Flank Pain
• U.A. shows pyuria and
bacteriuria
• Urinary signs:
frequency, urgency,
and burning
Treatment
• Antibiotics
• If severe enough to cause renal failure, then
renal dialysis is indicated
Glomerulonephritis
Transplant
Pulmonary Diseases
• Avoidance of triggers
• Inhaled steroids
– Budesonide,
fluticasone
• NSAIDS
– Cromolyn sodium,
nedocromil sodium,
– Zafirlukast,
montelukast
• Immuno-therapy
Chronic Bronchitis
Chronic Irritation
• Cigarette smoking
• Pollution
• Noxious fumes
• Chronic/recurrent infection
Pathology
• Cigarette smoking
• Alpha-1 anti-trypsin deficiency
– Usually a genetic defect
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
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.
Normal
Emphysema
Chest X-Ray
“Barrel” chest
COPD: Chronic Obstructive
Pulmonary Disease
A mixture of emphysema and
chronic bronchitis
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
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
COPD Complication: Cor
Pulmonale
• Lung transplant
•Decreased volumes
during PFT
•Lesion is in the alveolar
portion of the lung or the
chest wall
•Primarily occurs during
inspiration
Pneumoconiosis
• Prevention is best
– Symptoms may take 10-20 years of exposure
before they develop
• Oxygen therapy
• Lung transplant
ARDS
(Acute Respiratory Distress
Syndrome)
• Inhalation “insults”
– Noxious gases, aspiration of gastric contents
• Circulatory “insults”
– Shock from trauma/hemorrhage, sepsis
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
Manifestations
• Infection
• Aspiration
Pathology: Stage 1
Inflammation
Pathology: Stage 2
Consolidation
Bronchogenic Carcinoma
Squamous Cell Carcinoma
• Tumors develop in the
large, central airways
• Most common lung
cancer seen in
smokers
Adenocarcinoma
• Tumor arises from
glandular cells in
peripheral airways
Pathology
• 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
Diagnostic Tests
• Atherosclerotic
coronary arteries
• Deep veins of the legs
– Deep Venous
Thrombosis
• Fatty tissue from the
marrow of long bones
when fracture occurs
Etiology: Predisposing Factors
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
Diagnostic Tests
AH 120
The Pituitary, “The Master
Gland”
And, exopthalmos
Treatment
A. II only I. Tetany
B. I and III II. Muscle weakness
C. I and IV III. Increased blood
D. II and III levels of calcium
E. II and IV IV. Decreased blood
levels of calcium
Permanent destruction of
alveolar tissue leading to loss of
elastic recoil, over-inflation of
alveoli, and loss of alveolar septa
best describes:
A. COPD
B. Asthma
C. Emphysema
D. Chronic bronchitis
E. Pneumonia
A bacterial infection in the renal
pelvis and interstitial tissue best
describes:
A. Glomerulonephritis
B. Uremia
C. Pyelonephritis
D. Cystadenoma
E. Renal tubular necrosis
Airway changes that occur with
chronic bronchitis include:
A. I and IV I. Weak airways that
B. II and III tend to collapse
during exhalation
C. I, II and III II. Mucus gland
D. II, III, and IV hypertrophy
E. I, II, III, and IV III. Loss of cilia
IV. Squamous
metaplasia of the
epithelium
Enlargement of the thyroid that
does not necessarily affect its
function best defines:
A. Goiter
B. Throma
C. Pheochromocytoma
D. Endoma
E. Outoma
A patient receiving INH
(Isoniazid) is probably be
treating for which lung disease?
A. Pneumonia
B. Coccidioidomycosis
C. Bronchogenic carcinoma
D. Tuberculosis
E. Asthma
What abnormality of pulmonary
function occurs with obstructive
pulmonary disease?
A. Reduced lung volumes
B. Reduced flow rate of gas during exhalation
C. Increased lung volumes
D. Increased flow rate of gas during exhalation
E. Inability to perform a breath holding maneuver
When renal function ceases, the
appropriate treatment is:
A. Hemodialysis
B. Blood transfusion
C. Renal resection
D. Drug therapy
E. Purchase of additional life insurance