Download Renal Diseases

Renal Diseases
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:
Inflammation of the renal pelvis and
interstitial tissue of the kidney
Etiology
Bacterial infection that often spreads
retrograde from the bladder (cystitis)
Common agents: E-Coli, Strep, and
Staph
Acute
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
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
Inflammation of the glomerulus
caused by a reaction to immune
complexes and complement
It can be acute or chronic
Etiology
Usually caused by a strep infection
Strep throat
Strep skin lesion
Pathology
• Immune complexes and compliment damage glomerular
membrane and cause it to become more permeable
• WBCs, RBCs , and plasma proteins pass into Bowman’s
capsule
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
Treatment
• Supportive treatment if acute
• If chronic, patient may eventually need
dialysis and/or transplant
Renal Failure
Failure of the kidney to adequately
remove waste products and maintain
fluid and electrolytes.
It can be an acute or chronic process
Etiology
• Damage due to disease processes, e.g.,
pyelonephritis , glomerulonephritis, etc
• Reduced renal blood flow (shock)
– Burns, trauma, dehydration
• Toxins
– CCL4, Hg, ethylene glycol
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
Treatment
Hemodialysis (for acute
or chronic failure)
Treatment (cont.)
Transplant
Pulmonary Diseases
May involve the airways and/or the
alveoli
Pulmonary Disease Is Classified
By the Effect on Pulmonary
Function
Restrictive Pulmonary Disease
• Decreased volumes during PFT
• Lesion is in the alveolar portion of the lung
or the chest wall
• Primarily occurs during inspiration
Obstructive Pulmonary Disease
• Decreased flow rates during PFT
• Lesion is usually in the airways
• Primarily occurs during exhalation
Obstructive Diseases Caused By
Airway Inflammation
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
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
Examples of Airway
Inflammatory Diseases
The Common Cold
Usually viral in origin
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
Acute Bronchitis
(Chest Cold)
• Inflammation in the
trachea, main stem and
segmental bronchi
• Usually a
complication of a viral
infection
Asthma
Transient inflammation of the airways
ETIOLOGY
(“Triggers”)
•
•
•
•
•
•
Allergy
Infection
Stress/emotion
Noxious fumes
Cold air
Exercise
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
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!
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)
Prevention
• Avoidance of triggers
• Inhaled steroids
– Budesonide,
fluticasone
• NSAIDS
– Cromolyn sodium,
nedocromil sodium,
– Zafirlukast,
montelukast
• Immuno-therapy
Chronic Bronchitis
Productive cough for at least three
months of the year during a two year
period
Etiology
Chronic Irritation
• Cigarette smoking
• Pollution
• Noxious fumes
• Chronic/recurrent infection
Pathology
• Metaplastic change: ciliated, columnar epithelium
becomes squamous and non-ciliated
• Hyperplasia/hypertrophy of goblet cells
• Weakened, fibrotic airways that collapse easily
Emphysema
Hyperinflation of alveoli with
destruction of alveolar septa,
pulmonary capillary bed, and elastic
tissue in alveolar wall
Etiology
• 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
Heart failure due to lung disease
• 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
Cor Pulmonale Signs &
Symptoms
• Enlarged right heart
• Jugular Venous
Distension (JVD)
• Ankle edema
• Arrhythmias
– Usually atrial
• Prone to pulmonary
infections
Maintain Oxygenation
(this may require continuous O2)
Other Treatment Options
• Lung transplant
• LVRS (Lung Volume Reduction Surgery)
– Resect the most damaged part of the lung(s)
Restrictive Pulmonary Disease
•Decreased volumes
during PFT
•Lesion is in the alveolar
portion of the lung or the
chest wall
•Primarily occurs during
inspiration
Pneumoconiosis
Lung disease caused by inhalation of
dust particles
Etiology
Often due to occupational exposure
• Silicosis
• Coal Worker’s Pneumoconiosis
• Asbestosis
Pathology
• Prolonged inhalation
of dust particles
causing chronic
inflammatory response
in the alveoli
• Results in fibrosis
(scar tissue)
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
Treatment
• Prevention is best
– Symptoms may take 10-20 years of exposure
before they develop
• Oxygen therapy
• Lung transplant
ARDS
(Acute Respiratory Distress
Syndrome)
Also known as “shock lung”, acute
lung injury (ALI), post-traumatic
pulmonary insufficiency
Etiology
• 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
• 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
Treatment
• Support oxygenation and ventilation
– May require aggressive mechanical ventilation
– Even with aggressive treatment, mortality is
still around 50-60%
Pneumonia
Inflammation of the lung at the
alveolar level
Etiology
• Infection
• Aspiration
Pathology: Stage 1
Inflammation
Pathology: Stage 2
Consolidation
Alveoli are now filled with
inflammatory exudate.
Inflammation may spread to pleura
Pathology: Stage 3
Resolution
• Exudate in alveoli starts to break up
• Patient starts coughing productively to clear
the exudate and re-aerate the lung
Manifestations
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Fever & Chills
Dyspnea and S.O.B.
Hypoxia
Pleuritic chest pain
Abnormal breath sounds
Cough (only becomes productive during
resolution phase)
Treatment
•
•
•
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Drug therapy for infection
Fluids (P.O. or IV)
Oxygen for hypoxia
Respiratory care to get to resolution phase
Pulmonary Edema
Leakage of fluid from pulmonary
capillaries causing the fluid to
accumulate in the interstitium and
then to spill into the alveoli
Pulmonary Hemodynamics
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
Pathology
• Fluid accumulates in interstitium and
alveoli
• Leads to restriction and atelectasis and poor
gas exchange
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
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
Pulmonary Diseases That May
Cause Restriction, Obstruction,
or Both
Lesions may occur in airways and/or
alveoli
Tuberculosis
An infectious disease that usually
starts in the lung and spreads
throughout the body
Etiology: Mycobacterium
Tuberculosis
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
Pathology (cont.)
• If immune system is
overwhelmed, Tb
bacillus starts
“consuming” lung
tissue causing caseous
lesions
• May now spread to
other body organs
Manifestations
• No symptoms with initial infection
• If bacillus starts to spread and “consume” lung:
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Weight loss
Fatigue
Tachycardia
Night sweats
Hemoptysis
Hypoxia
• Note: these symptoms are very similar to lung
cancer
Diagnostic Tests
• Skin test
• CXR – look for either
calcified lesions or
caseous lesions
• Sputum Cytology
– Gram stain and AFB
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
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
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
Lung Cancer
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
• 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
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
Diagnostic Tests
• CXR, CT Scan, MRI
• Sputum cytology
• Biopsy
– May be needle biopsy or done by bronchoscopy
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
Pulmonary Embolism
A blood clot or fatty tissue that has
become free within the blood and
then gets trapped in the pulmonary
circulation
Etiology
• 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
• Lung Scan – compares distribution of ventilation
to perfusion
• Pulmonary angiogram
Prevention is best!
Thrombolytic drugs may
be used for both
treatment and prevention
Respiratory Failure
Any disease process (or injury) that
interferes with gas exchange
Oxygen levels drop and carbon
dioxide levels start to rise
Treatment: Mechanical
Ventilation
Endocrine Diseases
AH 120
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)
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
Acromegaly
(Hyperpituitarism AFTER
puberty)
• Hands, feet, and face
enlarge (especially
lower jaw)
• Coarse facial features
with thickened tongue
and curvature of the
spine
Treatment
Resect tumor (if accessible)
And/or radiation to shrink tumor
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
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
Simmond’s 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!
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
Thyroid Gland
Secretes thyroxin which regulates
metabolic rate
Hyperthyroidism
• Also known as Graves’ Disease
– Gland hypertrophies and produces too much
thyroxin
• Etiology:
– Benign or cancerous tumors
– Idiopathic
Signs & Symptoms
And, exopthalmos
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
Hypothyroidism
• Also known as Myxedema
• Etiology:
– Damage from disease, surgery or radiation
– Hypopituitarism
– Autoimmune reaction
• Pathology: decreased thyroxin causes
decrease in metabolic rate
Signs & Symptoms
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
Treatment
• Blood test to
determine presence
• Administration of
thyroxin
• If not diagnosed and
treated, there is
permanent impaired
mental and physical
development
Non-toxic Goiter
• Enlargement of thyroid
without affecting function
– May interfere with
swallowing and breathing!
• Etiology: iodine
deficiency, enzyme
deficiency, increased
hormone requirement
• Treatment:
Medications;sometimes
surgery
Adrenal Glands
Cortex secretes mineral corticoids
glucocorticoids and sex hormones.
Medulla secretes norepinephrine and
epinephrine
Hyperadrenalism
• Also known as Cushing’s 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
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
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
Hypoadrenalism
• Also known as Addison’s Disease
– Decreased glucocorticoids and mineral
corticoids
• Etiology:
– Autoimmune reaction that damages the gland
– Atrophy from steroid drug administration/abuse
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
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
Parathyroid Glands
Secrete parathormone which
regulates blood levels of calcium
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
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
Over production of parathyroid
hormone produces which of
these:
A.
B.
C.
D.
E.
II only
I and III
I and IV
II and III
II and IV
I. Tetany
II. Muscle weakness
III. Increased blood
levels of calcium
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.
B.
C.
D.
E.
COPD
Asthma
Emphysema
Chronic bronchitis
Pneumonia
A bacterial infection in the renal
pelvis and interstitial tissue best
describes:
A.
B.
C.
D.
E.
Glomerulonephritis
Uremia
Pyelonephritis
Cystadenoma
Renal tubular necrosis
Airway changes that occur with
chronic bronchitis include:
A.
B.
C.
D.
E.
I and IV
II and III
I, II and III
II, III, and IV
I, II, III, and IV
I.
Weak airways that
tend to collapse
during exhalation
II. Mucus gland
hypertrophy
III. Loss of cilia
IV. Squamous
metaplasia of the
epithelium
Enlargement of the thyroid that
does not necessarily affect its
function best defines:
A.
B.
C.
D.
E.
Goiter
Throma
Pheochromocytoma
Endoma
Outoma
A patient receiving INH
(Isoniazid) is probably be
treating for which lung disease?
A.
B.
C.
D.
E.
Pneumonia
Coccidioidomycosis
Bronchogenic carcinoma
Tuberculosis
Asthma
What abnormality of pulmonary
function occurs with obstructive
pulmonary disease?
A.
B.
C.
D.
E.
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
When renal function ceases, the
appropriate treatment is:
A.
B.
C.
D.
E.
Hemodialysis
Blood transfusion
Renal resection
Drug therapy
Purchase of additional life insurance