THE
HEART -
Seven major categories of cardiac diseases in
bold
I.
Congestive Heart Failure (CHF)
A.
The common end point of many different types of heart
disease
B.
Multisystem derangement that occurs, in most cases, when the
heart is no longer able to eject the blood delivered to it by the venous system
C.
Most common causes of left-sided cardiac failure
1.
Systemic HTN
2.
Mitral or aortic valve disease
3.
Ischemic heart disease
4.
Primary diseases of the myocardium
5.
(Leads to pulmonary edema)
D.
Most common cause of right-sided heart failure is left ventricular failure, other causes:
1.
Cor pulmonale
2.
Primary diseases of the pulmonary vasculature
3.
Pulmonic or tricuspid valve disease
4.
(Leads to nutmeg liver and anasarca)
E. Compensatory
mechanisms (compensated heart failure)
1.
Increased activity of sympathetic nervous system
2.
Hypertrophy
3. End-diastolic
pressure and volume increase®dilation
of heart
4.
Elongation and stretching of individual cardiac muscle
fibers (w/initial Frank-Starling response)
F. Decompensated heart failure
1.
Progressive decrease in myocardial contractility
2.
Declined cardiac output
3.
Decreased perfusion kidneys®renin-angiotensin system
4.
Increased aldosterone output
5.
Positive feedback
II.
Ischemic
Heart Disease - Coronary artery (heart) disease
A.
Most common cause atherosclerosis of coronary arteries
B.
Becomes symptomatic at 75% or greater occlusion
C.
In addition to fixed atherosclerotic plaques, myocardial
ischemia affected by superimposed lesions:
1. Acute
changes in morphology of chronic atherosclerotic plagues
a)
Fissuring
b)
Hemorrhage into the plaque
c)
Rupture with embolization of atheromatous debris
d) Increased risk of platelet aggregation
and thrombosis
2.
Local platelet aggregation
a)
Mechanical occlusion
b) Coronary
vasospasm [from endothelial mediators]®occlusion
3.
Coronary artery thrombosis®infarct
4. Coronary
artery spasm, associates with Prinzmetal’s (variant) angina
D.
Four resultant syndromes
1.
Angina Pectoris - intermittent chest pain caused by
reversible myocardial ischemia
a)
Typical (stable) angina pectoris (crushing feeling)
b) Prinzmetal's
(variant) angina (occurring at rest)
c) Unstable
(crescendo) angina pectoris
i.
With slightest exertion
ii.
a.k.a. preinfarction angina
2.
Myocardial Infarction - development of defined area of
myocardial necrosis caused by local ischemia
a)
Typically begin in the subendocardial region
b) Signs
and symptoms
i.
Severe, crushing substernal chest pain
ii.
May radiate
to neck, jaw, epigastrium, shoulder, left arm
iii.
Angina pectoris of several hour to days long
iv.
Dyspnea
v.
Cardiogenic shock
vi.
EKG abnormalities
c)
Complications of a transmural MI
i.
Papillary muscle dysfunction
ii.
Rupture of infarcted papillary muscle
iii.
External rupture of the infarct
iv.
Rupture of the intraventricular septum
v.
Mural thrombi
vi.
Acute pericarditis
vii.
Ventricular aneurysms
d) Subendocardial
MI restricted to the inner 1/3 of myocardium
e) Necrosis
**20-30 minutes
i.
Early coagulative begins by about 4-12 hours
ii.
Coagulative (pyknosis) necrosis in 12-18 hours
iii.
Complete coagulation necrosis in 24-72 hours
f)
Arteries most affected
i.
Left anterior descending coronary (40-50%)
ii.
Right coronary (30-40%)
iii.
Left circumflex coronary (15-20%)
g)
Lab findings in support of MI
i.
Creatine kinase®
CK-MB most specific indicator of MI
ii.
Lactate dehydrogenase
iii.
Serum levels of certain myocardial proteins
3. Chronic Ischemic Heart Disease with
congestive heart failure
4. Sudden
Cardiac Death
III. Hypertensive Heart Disease
IV.
Cor Pulmonale
- Heart disease caused by intrinsic pulmonary diseases
V.
Valvular
Heart Diseases
A. Rheumatic
Fever and Heart Disease
1. Etiology
group A streptococcal pharyngitis
2. Hypersensitivity
reaction against M proteins
3. Two to
three weeks allows antibody development
4. Antibodies
attack heart valves in multiple foci of inflammation, Aschoff bodies - containing a central focus of fibrinoid necrosis,
surrounded by a chronic mononuclear inflammatory infiltrate, and occasional
large histiocytes with vesicular nuclei and an abundant basophilic cytoplasm, Anitschkow cells
5.
Most commonly
affects left heart valves, mitral and
aortic
B. Calcific
Aortic Stenosis
1. Sclerosis and
calcification of the aortic valve most common cause of isolated aortic stenosis
in the U.S.
- a.k.a. degenerative calcific aortic
stenosis (DCAS)
2. Prophylactic
antibiotic therapy is important because death occurs 3-4 years after the onset
of symptoms
C. Mitral
Valve Prolapse
D. Nonbacterial
Thrombotic Endocarditis (NBTE)
1. Characterized
by the deposition of small masses of fibrin, platelets, and other blood
components on the leaflets of the cardiac valves
2. Lesions
of NBTE are sterile and contain no microorganisms
3.
Marantic
endocarditis - term for increased frequency of NBTE in cachectic (general
debility or wasting) patients
4. Lambl's
excrescences - resolved lesions that leave delicate strands of fibrous tissue
E. Infective
Endocarditis
1. Most
common organisms
a) Staphylococcus aureus
b) a-hemolytic
streptococci
c) HACEK
group (Haemophilus, Actinobacillus,
Cardiobacterium, Eikenella, and Kingella)
d) Staphylococci epidermidis
e) Gram
negative bacilli and fungi
2.
Acute - infection of valves by highly virulent organisms
such as Staphylococcus aureus
3. Subacute
- infection of previously abnormal valves by lower virulent organisms such as
a-hemolytic streptococci
F. Prosthetic
Cardiac Valves
VI.
Primary
Myocardial Diseases
A. Myocarditis
– inflammation
1. Infections
(viruses, chlamydia, rickettsia,
bacteria, fungi, protozoa, helminths)
2. Immune-mediated
reactions
3. Unknown
(sarcoidosis, giant cell myocarditis)
B. Cardiomyopathies
- heart disease resulting from a primary abnormality in the myocardium
1. Dilated
cardiomyopathy
a) Progressive
cardiac hypertrophy, dilation [of all chambers] and contractile (systolic) dysfunction
b) Result
of:
i.
Viral nucleic acids
ii.
Alcohol abuse
iii. Toxic
insult (cobalt)
iv.
Peripartum cardiomyopathy, occurs late in pregnancy or
post partum
v.
Idiopathic
2. Hypertrophic
cardiomyopathy
a) a.k.a.
asymmetric septal hypertrophy and idiopathic hypertrophic subaortic stenosis
b) Most
pronounced in the left ventricle and septum
c) Most
common in sudden unexplained death of young athletes
3. Restrictive
cardiomyopathy
a)
Primary
decrease in ventricular compliance, resulting in impaired ventricular filling
during diastole
b) Most
common cause - endomyocardial fibrosis Löffler’s syndrome - eosinophilic
endomyocardial fibrosis
i.
Proteins
released from degranulating eosinophils
ii.
Atria typically dilate
iii. Endocardium
thickened and opaque
c) Also
caused by cardiac amyloidosis, hemochromatosis and radiation injury
d) Stiff
and inelastic ventricle that can fill only with great effort
VII. Congenital Heart Disease
A. Left-to-Right
Shunts - most common type of CHD Cyanosis
is not an early feature, but
it may occur late
1. Atrial
septal defects
2. Ventricular
septal defects - most common type of L®R
3. Patent
ductus arteriosus
B. Right-to-Left
Shunts **Cyanosis is an early feature: results from poorly oxygenated
blood from the right side entering directly into the arterial circulation
1.
Tetralogy of
Fallot - most common cause of cyanotic
CHD
2. Transposition
of the great arteries - incompatible with life
C. Congenital
Obstructive Lesions
1. Coarctation
of the aorta
a) Fairly
common
b) Two
types
i.
Preductal (infantile) - congestive
heart failure, selective cyanosis
lower extremities, weak femoral pulse
ii.
Postductal - clinicals in
older children and adults; hypertension of the upper extremities (resulting
from low perfusion kidneys®renin-angiotensin
activation), low BP in lower extremities, arterial insufficiency in legs
(intermittent claudication)
VIII.
Pericardial Diseases
A. Pericarditis
1. Acute
P~ (a.k.a. shaggy heart, bread and butter pericarditis)
a) Viruses
most responsible, also SLE, rheumatic fever, and metastases
b) Uremia
most common systemic disorder
2. Chronic
P~
a) Formation
of delicate adhesions to dense, fibrotic scars that obliterate the pericardial
space
b) Can
lead to constrictive pericarditis
B. Pericardial
Effusions
1. Serous
- CHF and hypoalbuminemia
2. Serosanguineous
- blunt chest trauma, malignancy
3. Chylous
- lymphatic obstruction
4. Hemopericardium
- rupture aortic aneurysm, myocardial infarcts, penetrating injury
5. Leads
to cardiac tamponade and death
IX.
Cardiac Tumors
A. Metastatic
Neoplasms
1. Most
common
2. Most
often involves the pericardium
3. Most
often come from the lung and breast, malignant melanomas, and hematopoietic
malignancies
B. Primary
Neoplasms
1. Rare
2.
Most common
are myxomas, lipomas, cardiac rhabdomyomas
I.
Note general properties of endothelial cells and vascular
smooth muscle
II.
Arterial disorders
A. Arteriosclerosis
- thickening and inelasticity of arteries
1. Atherosclerosis
- most predominant form of arteriosclerosis
a) First
world nation predominant
b) Constitutional
risk factors - immutable (major non-modifiable)
i.
Age
ii.
Sex
iii. Familial
predisposition
c) Acquired
risk factors - major modifiable
i.
Hyperlipidemia
ii.
Hypertension - 140/90
iii. Cigarette
smoking
iv.
Diabetes
d) Soft
risk factors - minor modifiable
i.
Insufficient physical activity
ii.
Stressful life style (type a personality)
iii. Obesity
iv.
Use of oral contraceptives
v.
Hyperuricemia
vi.
High carbohydrate intake
vii. Hyperhomocysteinemia
e) Plaque
formation: endothelial dysfunction,
monocyte adhesion and infiltration, smooth muscle proliferation,
extracellular matrix deposition, lipid accumulation, and thrombosis
f) Morphologies
i.
Fatty dot - intimal discoloration
ii.
Fatty streak - elongated fatty dots
iii. Atheroma
- mainly intracellular lipid with a core of extracellular lipid
iv.
Fibrofatty atheroma - lipid core and fibrotic layer singly
or layered or calcific
v.
Atheromatous
plaque - hallmark of arteriosclerosis
2. Mönckeberg’s
medial calcific sclerosis
3. Arteriolosclerosis
- see b. Hypertension
B. Hypertension
and hypertensive vascular disease
1. Potential
mechanisms ®
aberrations of normal regulatory processes.
Arterial HTN occurs when changes develop that alter the relationship between
blood volume and total arterial resistance
2. 1° º idiopathicº140/90º[essential]
hypertension
a) Genetic
factors
b) Environmental
factors
3. 2° º
result of another condition
4. Benign
º
stable, modest HTN w/o MI or CVA
5. Malignant
º ?/120 BP; rapidly rising; death in 1-2
years; 1° or 2°
6. BP =
cardiac output x peripheral resistance
a) CO
results from volume; primarily by sodium control
b) PR
results from lumen size
i.
Vasodilators
ii.
Vasoconstrictors
c)
Renin (JGM
ce11s) ® angiotensin I (plasma) ® angiotensin
II (lung)
i.
Affects pr by causing vasoconstriction of VSC
ii.
Affects co by
stimulating aldosterone secretion
7. Vascular
pathology in HTN
a) Most
predominant in the kidneys [and other organs]
b) Hyaline
arteriolosclerosis - homogeneous, pink, hyaline thickening of arteriole walls
i.
Frequent in elderly
ii.
Benign nephrosclerosis
c) Hyperplastic
arteriolosclerosis
i.
Associated more with malignant HTN
ii.
Onion-skin, concentric, laminated thickening of arteriole
wall
iii. Necrotizing
arteriolitis - deposits of Fibrinoid and acute necrosis of vessel walls
C. Vasculitis
- inflammatory involvement of artery, vein, or venule
1. Polyarteritis
Nodosa (pan) - panmural acute necrotizing arteritis with fibrinoid necrosis,
neutrophil and eosinophil infiltration, and extension into adventitia
a) Medium
to small arteries in any organ (except lung)
b)
Sharply
segmental lesions of nodular aneurysmal dilation
c) GI
tract, liver, kidney, pancreas, muscles, other
d)
May coexist
in different or within the same vessel(s)
2.
Wegener's
granulomatosis - acute and chronic (sometimes granulomatous) angiitis with
prominent eosinophils and occasional giant cells in association with
extravascular granulomas
a)
Small to
medium-sized arteries
b)
Upper and
lower respiratory tracts; occasionally eye, skin, heart
c) Necrotizing granuloma
3. Microscopic
polyangiitis - necrosis and neutrophilic infiltration of venules with
leukocytoclasis -(fragmented neutrophils that follow vessel wall)
a) Venules,
capillaries, arterioles
b) Widespread,
but mostly skin
4. Temporal
(giant cell, cranial) arteritis - chronic mononuclear inflammatory
infiltration, mostly in inner half of the media, with giant cells and granuloma
formation
a) Elastic
tissue - rich major arteries of head
b) Head,
including ocular and intracranial vessels; uncommonly systemic
5. Takayasu's
arteritis (pulseless disease) - chronic vasculitis that affects principally the
aorta and its main branches and sometimes the pulmonary arteries
a) Mostly
women; mostly upper extremity
b) Once
erroneously Asian origin - now known globally
c) Thickening
aortic wall resulting in lack of pulse
6. Kawasaki's
disease - acute and chronic infiltration mainly with lymphocytes and
macrophages, and with endothelial cell necrosis and immunoglobulin deposition
a) Acute
febrile illness of infancy
b) Small
and medium-sized arteries
c) Skin,
ocular and oral mucosa, coronary arteries, may be widespread
7. Thromboangiitis
Obliterans (Buerger’s disease) -sharply segmental acute and chronic inflammatory
infiltration of arteries and veins, often with giant cells, granulomas,
intravascular thrombi containing microabscesses, and later perivascular
fibrosis trapping nerve trunks
a) medium-sized
and small arteries and veins
b)
extremities -
principally tibial and radial arteries
c) male
cigarette smokers age 25-50
d) often
preceeded by Raynaud’s phenomenon
D. Aneurysms
- dilation of arteries or veins that develop wherever there is marked weakening
of the vessel wall
1. Anatomical
classifications
a) Saccular
- balloon-like
b) Fusiform
- general widening to general narrowing
c) Cylindroid
- sudden widening to sudden narrowing
d) Berry-shaped
- little ball
e) saccular
berry - circle of Willis
2. Etiological
classifications
a) Atherosclerotic
(abdominal) aneurysm
i.
Most common cause of aneurysm
ii.
Clinical complications
1) Occlusion
of nearby arteries
2) Embolization
3) Tumor
stimulation
4) Erosion
of adjacent structures
5) Rupture
b) Syphilitic
Aortitis and aneurysm
i.
Tertiary stage of syphilis
ii.
Always thoracic
iii. Causes
narrowing of vasa vasorum aorta
iv.
Clinical complications
1) Occlusion
of airways
2) Difficulty
in swallowing
3) Persistent
brassy cough (rec. lar. N.)
4) Pain
from bone erosion
5) Cardiac
disease - valvular insufficiency
c) Aortic
Dissection (dissecting hematoma)
i.
Common in males age 40-60 with HTN
ii.
Common in Marfan’s syndrome
iii. Clinical
complications
1) Double
barreled aorta
2) Cystic
medial necrosis
3) Atherosclerosis
4) Rupture
5) Hemorrhage
III.
Venous disorders
A.
Varicose veins
1.
Result from increased intraluminal pressure and loss of
support of vessel wall
2.
Clinical significance
a)
Pain
b)
Incompetent valves ® venous stasis ®
increasing pressure ® edema ® impaired circulation ® vulnerability to injury
i.
Trophic changes
ii.
Stasis dermatitis
iii.
Cellulitis
iv.
Ulceration
v.
Thrombosis
vi.
Embolization
vii.
Bleeding
3.
Most common involvement
a)
Lower legs; superficial and deep (DVT)
b)
Hemorrhoids
c)
Esophageal varix
B.
Phlebothrombosis and thrombophlebitis - thrombi that arise
in DVT’s. Note: Trousseau's sign - migratory
thrombophlebitis; in patients with cancer, venous thromboses that appear
spontaneously in one site, only to disappear with subsequent thromboses in
other veins
IV.
Lymphatic disorders
A. Lymphangitis
- infections that spread
into the lymphatics
1.
GROUP A b-hemolytic
streptococci
2.
Red streaks and tenderness
B.
Lymphedema
1.
1°
a)
Isolated or congenital (familial)
b)
Milroy’s disease - incomplete lymphatics; mostly lower
extremity
c)
Lymphedema praecox
i.
Affects mostly females age 10-25
ii.
Starts distal and moves proximal
2.
2° - develop
in association with inflammation or cancer
a)
Postinflammatory scarring of lymphatic channels
b)
Spread of malignant neoplasms
c)
Radical surgical procedures
d)
Postradiation fibrosis
e)
Filariasis
C.
Clinical notes
1.
Edema occurs distal to lymph obstruction
2.
Edema can
lead to interstitial swelling and fibrosis - peau d'orange
V.
Vascular tumors
A.
Hemangiomas
B.
Glomangioma (glomus tumor)
C.
Hemangioendothelioma and angiosarcoma
D.
Kaposi's sarcoma (KS) - three types
1.
Classic KS
a)
Affects elderly men (predominantly Jewish)
b)
Relatively indolent
c) Red-blue
inflamed-looking lesions distal lower extremities
d)
Become more numerous and centripetal and nodular
e)
Three stages
i.
Patch - pink/red/purple macule(s)
ii.
Plaque - raised,
larger, violet
iii.
Nodule - mitotic
presence
2.
African or endemic KS
a)
Same distribution as Burkitt’s lymphoma
b)
Primarily young black males
3.
Epidemic KS
a)
Seen in aids
b)
90-95% in homosexual men
c)
Incidence is declining
d)
Locally produced growth factors causing unchecked growth of
cells
THE
LUNGS
I.
Atelectasis (collapse)
A.
Resorption a -
obstruction prevents air from reaching distal airways
B.
Compression a
(a.k.a. passive or relaxation a~) -associates with accumulations within
the plural cavity that mechanically collapse the lung
C.
Microatelectasis (a.k.a. nonobstructive a~)
- loss of lung expansion due to a complex set of events (i.e. loss of
surfactant)
D.
Contraction a (a.k.a. cicatrization) - fibrotic changes in lung or pleura
hamper expansion and increase elastic recoil
II.
Obstructive and restrictive lung diseases - general terms
A.
FVC - forced vital capacity
B.
FEV1 - forced expiratory volume at 1 second
(rate)
C.
FEV1/FVC -
ratio used to compare obstructive with restrictive
III. Obstructive
lung diseases - FVC is normal; FEV1 decreased;
FEV1/FVC resultantly decreased
A.
Asthma - episodic, reversible bronchospasm resulting from an
exaggerated bronchoconstrictor response to various stimuli
1.
Triad of asthma - DCW (dyspnea, coughing, wheezing)
2. Most
striking macroscopic finding is occlusion of bronchi and bronchioles by thick,
tenacious mucous plugs that contain Curschmann's
spirals - whorls off shed epithelium. Numerous eosinophils and Charcot-Leyden
crystals (collections of crystalloids
made up of eosinophil proteins) are also present
3. Status
asthmaticus - severe
paroxysm that does not respond to therapy and persists for days and even weeks
4.
Extrinsic
a)
Type I hypersensitivity reaction from extrinsic antigen
b)
Three types
i.
Atopic asthma
1)
Most common extrinsic
2)
Key
players - IgE, mast cells, and eosinophils
ii.
Occupational asthma
iii.
Allergic bronchopulmonary aspergillosis
5.
Intrinsic
a)
Nonimmune triggering mechanisms
b) Caused by aspirin, infections, cold,
stress, exercise
B.
COPD
1.
Emphysema
a) Permanent
enlargement of airspaces distal to the terminal bronchioles accompanied by
destruction of their walls
b)
Three types
i.
Panacinar (panlobular) - apical lung
ii.
Centriacinar (centrilobular) - lower lung
iii. Distal acinar (paraseptal) - adjacent
to pleura
c) There is a clear association between
heavy cigarette smoking and emphysema
i.
Smokers accumulate neutrophils and
macro's in alveoli
ii.
Neutrophil release elastase b/c of smoking
iii. Macro’s elastase activity enhances b/c
of smoking
iv.
Smoke oxidants inhibit antielastase activity
d) Occurs by excess protease or elastase
activity unopposed by appropriate antiprotease/antielastase regulation. This results in elastic tissue damage and
emphysema
e) Pink
puffers - b/c of
prominent dyspnea and adequate oxygenation of hemoglobin - often barrel-chested
f) Blue
bloaters - emphysema
with chronic bronchitis, with history of recurrent infections with purulent
sputum, retain co2 and become hypoxic and cyanotic - often obese
2.
Chronic bronchitis
a) Persistent
productive cough for at least 3 consecutive months in at least 2 consecutive
years
b) Forms:
simple, chronic mucopurulent, chronic, asthmatic, chronic obstructive
C.
Broncheictasis
1.
Permanent dilation of bronchi and bronchioles due to
destruction of the muscle and elastic supporting tissue, resulting from or associated
with chronic necrotizing infections
2. Causes:
a)
Bronchial obstruction
b) Congenital
or hereditary conditions
i.
Cystic fibrosis - most common cause in U.S.
ii.
Immunodeficiency
iii. Kartagener's
syndrome - abnormalities of cilia
c)
Necrotizing, or suppurative, pneumonia
IV.
Restrictive lung diseases - FVC is reduced; FEV1 normal or decreased; FEV1/FVC
resultantly near normal
A.
Extra-pulmonary disorders - affect the ability of the chest
wall to act as bellows (obesity, kyphoscoliosis)
B. Characterized
by reduced compliance
C. Acute
restrictive lung diseases – ARDS
1.
Acute onset of respiratory distress
2. Decreased
arterial oxygen pressure
3. Decreased
lung compliance
4. Development
of diffuse pulmonary infiltrates on x-ray
5. Diffuse
alveolar damage is the morphologic counterpart
6. Most
characteristic finding - hyaline membranes, particularly lining the distended
alveolar ducts
7. leads
to honeycomb lung
D. Chronic restrictive lung diseases
1. Idiopathic pulmonary fibrosis (IPF)
2. Sarcoidosis
a) Multisystem disease of unknown cause
characterized by noncaseating granulomas in many tissues and organs
b) Diagnosis is one of exclusion
i.
Patients
manifest cutaneous anergy to common test antigens
ii.
T lymphocytes
often decreased
iii.
Bronchoalveolar lavage shows increased
T lymphocytes
iv.
Normal number
B cells, but excess Ig's
c)
Lymph
node (hilar and paratracheal) involvement; X-ray shows noncaseating granulomas (key suggestive pathology)
d) Lung involvement with pulmonary
infiltrates and hilar adenopathy x-ray visible
e) Skin lesions
f) Eye, lacrimal and salivary glands with
iritis or iridocyclitis, inflammation w/o tears, and Mikulicz's syndrome -
combined uveoparotid involvement
g) Spleen and liver granulomas
h) Other
3. Hypersensitivity pneumonitis
a) Immunologically mediated inflammatory
lung disease primarily affecting the alveoli - allergic alveolitis
b) Acute reaction with fever, cough,
dyspnea and constitutional complaints
c) Chronic disease with insidious onset of
cough, dyspnea, malaise, and weight loss
4. Diffuse pulmonary hemorrhage syndromes
a) Goodpasture7s syndrome -
Crescentic glomerulonephritis and hemorrhagic interstitial pneumonitis
b) Idiopathic pulmonary hemosiderosis
c) Vasculitis-associated hemorrhage
V.
Vascular lung
diseases
A. Pulmonary thromboembolism, hemorrhage,
and infarction
1. More than 95% of all pulmonary emboli
arise from DVT's, popliteal and above
2. The majority are non-symptomatic, or
clinically silent
3. Less than 5% of cases result in sudden
death
4. Patients
that experience one P E have a 30% chance of a second
5. Nutrient sources
a) Pulmonary arteries
b) Bronchial arteries
c) Directly from alveolar air
B.
Pulmonary hypertension
and vascular sclerosis
VI.
Pulmonary infections
A.
Acute bacterial pneumonias
1. Lobar
pneumonia - contiguous airspaces of part or all of a lobe are homogeneously
filled with an exudate visible on radiographs as a lobar or segmental
consolidation (solidification)
a) S.
pneumoniae (serotype 3) produce 90% of lobar
pneumonias; also Klebsiella, mycoplasmas,
Legionella pneumophila
b) Four
stages: congestion, red (liver-like) then gray (dry, gray, and firm)
hepatization, and resolution
2. Bronchopneumonia - implies a patchy
distribution of inflammation that generally involves more than one lobe
a)
Distribute in yellow patches throughout the lung
b) Haemophilus influenzae, S. aureus, P.
aeruginosa, Moraxella catarrhalis
3.
Complications:
abscess, empyema, develop to fibrous tissue, meningitis, arthritis or infective
endocarditis Note: aspiration bronchopneumonia
B. Primary atypical pneumonias; mycoplasmas apparently the cause
C. Actinomycosis
and Nocardiosis
D. TB
1.
TB infection
a)
Seeding of some focus with organisms that may or may not cause
pathology
b) Detectable
by Mantoux test
c) A
positive TB test signifies cell-mediated hypersensitivity to TB antigen
2.
Primary TB
a) Develops in a previously unexposed,
unsensitized person
b) Ghon
focus - 1-1.5cm area of gray-white inflammat6ry consolidation in lung
c) Ghon
complex - combination of parenchymal lesion and nodal involvement
d) Sometimes
cavitates and spreads thru airways or lymphatics to multiple lung sites
e) Miliary
TB - spread of TB through blood
3.
Secondary TB (reactivation TB)
a)
Pattern of TB that arises in a previously sensitized host
b) Classical localized to the apex of one
or both upper lobes; AIDS - cavitation is distinctly uncommon and mediastinal
lymphadenopathy usually occurs
c) Miliary
pulmonary disease - drain thru lymphatics into lymphatic ducts to right heart
and into pulmonary arteries and lungs
d) Pott's disease - TB of
the vertebrae
E.
Fungal infections
1.
Histoplasmosis
a)
Ohio, Mississippi, Appalachian
b) Mimics
TB clinically and histologically
c) Infect
and multiply in phagocytes
2.
Coccidioidomycosis
a) C.
immitis - Valley
fever; endemic to San Joaquin Valley
b) Like
histoplasmosis and TB:
i.
Asymptomatic pulmonary infection
ii.
Progressive pulmonary disease
iii. Miliary
disease
3.
Candidiasis
4. Other
Fungal infections
F.
Lung abscess
G. CMV
H. Pneumoncystis
pneumonia
VII.
Lung tumors
A.
"Coin" lesion - hamartoma that shows up on x-ray
B. Bronchogenic
carcinoma
1.
Four types in two categories
a)
NSCLC (non-small cell lung CA)
i.
Squamous cell carcinoma - often associates with
hypercalcemia and correlates with smoking
ii.
Adenocarcinoma - common among nonsmoking women under age 40, often
associate with hematologic syndromes
iii. Large
cell undifferentiated carcinoma
b)
SCLC (only small cell carcinoma)
i.
Strong connection with smoking
ii.
Oat
cell carcinoma - small, dark, round-to-oval,
lymphocyte-like cells that have scant cytoplasm and hyperchromatic nuclei,
among which mitoses are numerous
iii. Rarely resectable
iv.
Best genetic alteration description for this type of cancer:
1)
Amplification of the myc
family of oncogene
2) Mutational
activation of tumor suppressor genes p53 and Rb
3) Mutations of K-ras associate with adenocarcinomas, not SCLC's
C.
Bronchial carcinoid - not a carcinoma, just a slow-growing
lesion, usually in the hilar region
VIII.
Pleural lesions
A. Malignant
mesothelioma - amphibole (long, straight) asbestos exposure
B. Pleural
effusion and pleuritis
1. Hydrothorax
- transudate effusion
2. Result
from microbial invasion, cancer, bronchogenic infarct, and viral pleuritis
C. Pneumothorax,
hemothorax, and chylothorax
IX.
Lesions of the upper respiratory tract
A. Acute
infections
B. Nasopharyngeal
carcinoma
C. Laryngeal
tumors
1. Nonmalignant
lesions – polyps
2. Carcinoma
of the larynx
THE KIDNEYS
I. Clinical manifestations of renal diseases
A. Azotemia
- elevated BUN and creatinine
B. Acute nephritic syndrome -
glomerular syndrome dominated by the acute onset of usually grossly visible
hematuria, mild to moderate proteinuria, and HTN
C. Nephrotic syndrome - heavy
proteinuria, hypoalbuminemia, severe edema, hyperlipidemia, and lipiduria
D. Asymptomatic
hematuria or proteinuria - subtle or mild glomerular abnormalities
E. Acute renal failure - dominated
by oliguria with recent onset of azotemia
F. Chronic renal failure - prolonged clinicals of uremia
G. Urinary
tract infection
H. Nephrolithiasis
II. Glomerular diseases
A. 1°
glomerulonephritis - kidney is the only or predominant organ involved
1. Acute
diffuse proliferative glomerulonephritis
2. Rapidly
progressive (crescentic) GN
3. Membranous
GN
4. Lipoid
nephrosis (minimal change disease)
5. Focal
segmental glomerulosclerosis
6. Membranoproliferative
GN
7. IgA
nephropathy
8. Chronic
GN
B. 2°
glomerulonephritis diseases that effect the kidney secondarily
1. SLE
2. Diabetes
mellitus
3. Amyloidosis
4. Goodpasture's
syndrome
5. Polyarteritis
Nodosa
6. Wegener’s
granulomatosis
7. Henoch-Schönlein
purpura
8. Bacterial
endocarditis
C. Pathogenesis
1. Circulating
immune complex nephritis
a) Ag
+ Ab complex in plasma deposits in a granular manner between the endothelium
and basement membrane
b) Granular
immunoflourescence of GBM
2. Immune
complex nephritis in situ
a) Anti-GBM nephritis
i.
Ab
in plasma enters the basement membrane and binds with Ag within basement
membrane
ii.
Smooth
immunoflourescence of GBM
b)
Heymann's
nephritis
i.
Ab in plasma
passes through basement membrane and binds with Ag in the pedicels
ii.
Granular immunoflourescence
of GBM
3.
Cell-mediated
immune glomerulonephritis
4.
Mediators of
immune injury (reduced filtration rate)
a)
monocytes and
macrophages
b)
Platelets
c)
Resident
glomerular cells
d)
Fibrin-related
products
5.
Other
mechanisms of glomerular injury
a)
Epithelial
cell injury
b)
Renal
ablation glomerulopathy
D. Glomerular syndromes and disorders
1.
Nephrotic syndrome
a)
Minimal
change disease (lipoid nephrosis) glomeruli that have a normal appearance under
the light microscope but disclose diffuse
loss of visceral epithelial foot processes when viewed with the electron
microscope
b)
Membranous
glomerulonephritis
Presence of subepithelial immunoglobulin-containing deposit along the GBM
c)
Focal
segmental glomerulosclerosis
Sclerosis affecting some but not all glomeruli and involving only segment of
each glomerulus
d)
Membranoproliferative
glomerulonephritis
i.
Altered
basement membrane and mesangium and by proliferation of glomerular cells
ii.
Light
microscopy show a double-contour or "tramtrack" appearance resulting
from a splitting of the basement membrane by mesangial cells
2.
Nephritic
syndrome - typically hematuria, oliguria,
and HTN
a)
Acute
proliferative glomerulonephritis
i.
a.k.a. Poststreptococcal or
Postinfectious glomerulonephritis, perhaps even Diffuse Proliferative
Glomerulonephritis
ii.
Smokey brown urine
b)
Rapidly progressive (crescentic) - Presence of crescents in most of the
glomeruli b/c or proliferation of parietal epithelial cells of Bowman's capsule
and monocytes/macrophages.
Common denominator - sever glomerular Injury
i.
Type I RPGN (Anti-GBM disease)
1) Idiopathic
2) Goodpasture's
syndrome
ii.
Type II RPGN (Immune complex-mediated
disease)
1) Idiopathic
2) SLE
3) Post
infectious
4) Henoch-Schönlein
purpura
iii.
Type III RPGN
(Pauci-immune or lack of Anti-GBM)
1) Idiopathic
2)
Wegener's
granulomatosis
3)
Polyarteritis
c)
IgA
Nephropathy (Berger's disease)
i.
Most common causes of recurrent
microscopic or gross hematuria and most common glomerular disease worldwide
ii.
Hallmark is
deposition of IgA in the mesangium
d)
Hereditary
nephritis - Alport's syndrome
3.
Chronic
glomerulonephritis - by the time of presentation, glomerular changes so advance
that it is difficult to discern the nature of the original lesion
III. Diseases affecting
tubules and interstitium
A.
Tubulointerstitial
nephritis
1.
Acute
pyelonephritis
a)
Principle
causes: Enteric G(-) rods (E. coil,
Proteus, Klebsiella, Enterobacter, Pseudomonas)
b)
Two routes:
hematogenous and ascending from lower UTI
2.
Chronic
pyelonephritis and reflux nephropathy; common causes:
a) Chronic
obstructive pyelonephritis, recurrent infection superimposed on diffuse or
localized obstructive lesions leading to recurrent bouts of renal inflammation
and scarring
b)
Reflux
nephropathy, superimposition on a congenital vesicouretral reflux and
intrarenal reflux
3.
Drug-induced
interstitial nephritis
a)
Acute
i.
Adverse
reaction to a constantly increasing number of drugs
ii.
Synthetic
penicillins, synthetic antibiotics, diuretics, NSAIDS, misc.
b)
Analgesic
nephropathy
i.
Often
associates with renal papillary necrosis
ii.
Serious
complication - transitional cell carcinoma of renal pelvis
B.
Acute tubular
necrosis
1.
Destruction
of tubular epithelial cells and by acute suppression of renal function (oliguria)
2.
Most common
cause of Acute Renal Failure (ARF)
3.
Ischemic ATN;
mismatched blood, myoglobinuria
4. Nephrotoxic
ATN; poisons (heavy metals), organic solvents, drugs
IV.
Diseases involving blood vessels
A. Benign
nephrosclerosis (hyaline arteriolosclerosis)
B. Malignant
HTN and malignant nephrosclerosis (hyperplastic arteriolosclerosis)
C. Thrombotic
microangiopathies; microangiopathic hemolytic anemia, thrombocytopenia, and
renal failure
VI.
Cystic diseases of the kidney
A. Simple
cysts; generally innocuous
B. Autosomal
dominant (adult) polycystic kidney disease (APKD) Multiple expanding cysts of
both kidneys that ultimately destroy the intervening parenchyma
C. Autosomal
recessive (childhood) polycystic kidney disease Multiple epithelium-lined cysts
in the liver as well as proliferation of portal bile ducts
VII. Urinary
outflow obstruction
A. Renal
stones (urolithiasis)
1. Most
common: calcium oxalate mixed with
calcium phosphate
2. Factors
important in developing stones
a) Increased
urine concentration of the stone's constituents, to that it exceeds their
solubility in urine
b) Excess
calcium absorption in gut w/o hypercalcemia
c) Hypercalcemia
with excess excretion into UTI b/c of:
i.
Hyperparathyroidism
ii.
Vitamin D intoxication
iii. Sarcoidosis
d) Excessive
excretion of uric acid in urine
3. Magnesium
ammonium phosphate (struvite) stones - alkaline urine, owing to UTI's
4. May
produce unilateral or bilateral
5. Staghorn
calculi - in renal calyceal system
B. Hydronephrosis
1. Dilation
of the renal pelvis and calyces
2. Congenital;
atresia, valve formations, compression
3. Acquired;
foreign bodies, tumors, inflammation, neurogenic, pregnancy
VIII.
Tumors
A. Triad
of symptoms
1. Painless
hematuria
2. Long-standing
fever
3. Dull
flank pain
B. Renal
cell carcinomas
1. Most
common tumor in adults
2. Greater
frequency in cigarette smokers, and familial forms
3. von
Hippel-Lindau syndrome (VHL), hemangioblastomas of the CNS and retina; often
develop bilateral, often multiple renal cell carcinomas
C. Wilms'
tumor; childhood kidney tumor
D. Tumors
of the urinary bladder and collecting system
1. Papillomas
2.
Carcinomas