Mod 2: Clinical Correlates Flashcards
Amyloidosis
abnormal extracellular PROTEIN deposits (misfolded proteins form fibrillar aggregates) originally thought to be polysaccharides/starch
- -difficult to degrade/phago
- -accumulate –> tissue/organ loss of architecture/loss of function
Immunocyte dyscrasia
abnormal B cell proliferation/activation
- -excessive production of Ig light chains (Bence Jones proteins)
- -renal, splenic, lymph node pathologies (Ig clogs up organs where fluid passes through)
Dyscrasia
abnormal component of the blood
eucrasia = health
dyscrasia = disease
Why is there a change in sense of smell with age?
Loss of olfactory epithelium SA
Loss in number of CELL BODIES and NEURONS in OLFACTORY BULB
stem cells –> mature cells DECREASES with age
DEC in OBP
Blood vessels that can circumvent aortic coarctation (narrowing of aorta)
anastamoses b/w ant and post intercostal aa
Sentinel node biopsy
radio-opaque dye injected into cancer site and tracked to the first lymph node of drainage, using radiography
That node, and any other nodes nearby are biopsied or removed
Breast cancer –> check for metastasis in axillary lymph node
Thoracic Outlet Syndrome
major obstruction of vessels/nerves emerging from the sup thoracic aperture (usually at root of neck)
Trauma inflames scalene muscles – compresses brachial plexus, vessels
Remove scalenes and 1st rib to treat
Pneumothorax
entry of air
results in collapsed lung
ex. bullet punctures thoracic wall and parietal pleura + lung and visceral pleura — allows air in
Hemothorax
entry of blood
does not cause lung to collapse
Thoracocentesis
Pleural tap
needle inserted at mid-axillary line in 9th intercostal space (low enough to avoid hitting lung tissue)
needle must be inserted a little sup to 10th rib to avoid intercostal VAN and its collateral branches
Referred pain
happens b/c visceral sensation travels back to CNS via the exact routes of sym efferent input
In dorsal horn of SC, indiv cell bodies receive input from both visceral and somatic structures, confusing the brain as to where the pain is actually located –> referred pain
–pain is felt on body wall locations innervated by corresponding spinal level (dermatomes)
Dermatome corresponding with heart
appendix
heart: T1-T5
appendix: T10
CC16
diagnostic marker (clara cell secretory protein) low levels indicate tissue injury
Variations in branches from aortic arch
L common carotid originates from brachiocephalic trunk (27% of people)
R brachiocephalic does not exist so R common carotid and R subclavian branch directly from aortic arch
L brachiocephalic a on left side branches into L common carotid and L subclavian vessels
Aortic aneurysm
Localized dilation of aorta
Weakened aortic wall
Pt complains of chest pain that radiates to back
Seen on angiogram (radiograph)
Coarctation of aorta
narrowing (stenosis) of aorta – near site of ligamentum arteriosum
Collateral vessels may become enlarged and pulsate in intercostal spaces
Aortic aneurysm vs coarctation
aneurysm: localized dilation
coarctation: narrowing (stenosis)
Phrenic n and breathing – neck injuries
If SC damaged below C3-C5, still able to breath
If damaged above this region, no innervation to diaphragm, intercostal muscles – cannot breathe
Recurrent laryngeal nerve damage/injury
alters voice – recurrent laryngeal nn supply intrinsic muscles of larynx and swallowing safety
damaged by:
–bronchogenic/esophageal carcinoma
–enlargement of medaistinal lymph nodes
–aortic aneurysm
–cardiac surgery (especially in infants)
Phrenic nerve injury/block
paralysis of diaphragm
- -injury
- -block (during lung operation)
Aspiration of foreign bodies
enter Right bronchus (b/c wider, shorter, and more vertical)
Cough reflex
elicited when foreign body makes contact with carina (which is covered by mucous membrane and is very sensitive to tactile stimulation)
Bronchogenic carcinoma
enlargement of tracheo-bronchial lymph nodes
alter position of and immobilize the carina
–morphological changes in carina are diagnostic signs
Hiatal hernia
protrusion of stomach into mediastinum through the esophageal hiatus of diaphragm
–after middle age due to weakening of diaphragm and widening of esophageal hiatus
Chylothorax
blockage of cisterna chyli
lymph accumulates in pleural cavity
ACE inhibitors
prescribed for hypertension
regulates levels of angiotensin II
Emphysema
permanent ENLARGEMENT of air spaces distal to terminal bronchioles
Causes:
progressive, irreversible destruction of elastic tissue of alveolar walls
–destroyed by elastase (neutrophils)
–neutrophils secrete elastase in response to chronic exposure of chemicals/toxins OR genetic alpha1-antitrypsin deficiency
–alpha1-antitrypsin neutralizes elastase
–more neutrophils, more elastase –> elastic tissues destroyed
Without elastic fibers, no tissue recoil
Adjacent alveoli confluent, creating large air spaces
Steps of emphysema development
Stimulus inc macrophages – secrete chemoattractants for neutrophils
Neutrophils accumulate and release elastase
alpha1-antitrypsin neutralizes elastase
Persistent stimulus inc neutrophils
Neutrophils release elastase
Serum alpha1-antitrypsin levels dec and elastase starts destruction of elastic fibers – emphysema
Damaged fibers cannot recoil
Centracinar emphysema vs panacinar emphysema
Centracinar: wall of RESP BRONCHIOLES destroyed by elastase/other proteases
–cigarette smokers
Panacinar: wall of RESP BRONCHIOLES, ALVEOLAR DUCTS, and ALVEOLI destroyed by elastase/other proteases (boundaries of structures is lost)
–alpha1-antitrypsin deficiency
Asthma
Inflammation of airways causing NARROWING of airways swelling/muscles tighten bronchus constricts the greatest amount of all airways cells produce excess mucus -- further narrows airways (goblet, clara) Causes: --allergens --resp infections --exercise --pollutants --genetics Treatments --corticosteroids --anticholinergics
What are the key WBC in emphysema?
Asthma?
Emphysema: macrophages –> neutrophils
Asthma: eosinophils (major basic protein causes airway damage)
Compare normal airway and airway with asthma
Normal
- -thin mucus layer
- -thinner lamina propria with few WBC
- -thin smooth m layer
- -fewer glands
Asthma
- -thick mucus
- -thicker lamina propria with high numbers of macrophages, mast cells, eosinophils, neutrophils, other WBC
- -thicker smooth m
- -more glands
Histopathology of a small airway in fatal asthma
Lumen occluded with mucus plug Goblet cell metaplasia Airway thickened Inc in basement membrane thickness Inc in airway smooth m thickness
Chronic bronchitis
chronic exposure to pollutants, pathogens,and other toxins –> inflammation and NARROWING of airway passages
very similar to asthma
-reversible
-narrowing of airways
-chronic bronchitis can be cured, but asthma cannot be cured
COPD
overlap of symptoms b/w emphysema, chronic bronchitis, and asthma
Emphysema: alveolar wall destruction, overinflation
Chronic bronchitis: productive cough, airway inflammation
Asthma: reversible obstruction, triggered by allergens, infection
Compare asthma/chronic bronchitis vs emphysema
Asthma/chronic bronchitis
- -reversible
- -narrowing of airways
- -mucus plugs
Emphysema
- -irreversible
- -dilation of airways
- -destruction of lung parenchyma
Neonatal respiratory distress syndrome (RDS)
Babies w/o sufactant --premature births --diabetic moms (high level of insulin -- antagonize effects of corticosteroids) Symptoms: --rapid breathing --nasal flaring --audible grunting --cyanosis Prevention: corticosteroids to mom expected to deliver 25-34 weeks gestation Treatment --artificial surfactant --warm, moist O2 --continuous pos airway pressure (CPAP) -- keeps airways open --breathing machine
Normal transition in breathing from fetal life
Rapid redirection of gas exchange from placenta to lungs
1. replace alveolar fluid with air
2. onset of regular breathing
3. increased pulmonary blood flow
Normal surfactant production during 35 weeks gestation
–Type II pneumocytes secrete
–induced by corticosteroids
Steps of Neonatal RDS development
- insufficient surfactant
- increased alveolar tension
- hypoventilation and CO2 retention
- dec blood flow to lung
- endothelial damage
- fibrin and dead Type I pneumocytes create hyaline membranes that further cause CO2 retention (alveolar interstitum)
Blue baby
venous blood circulates body rather than arterial blood – due to:
- -failure of pulmonary trunk and aorta to separate (could be due to problem with neural crest cells)
- -tetralogy of fallot
Problem with neural crest cell can lead to lack of … in fetus
lack of separation of pulmonary trunk and aorta
Atrial septal malformation
left to right shunt
Ventricular septal malformation
left –> right shunt
Persistent AV canal malformation
associated with others
AV valve malformation
reduced oxygenation
Semi-lunar valve stenosis
pulmonary hypertrophy and cardiac failure
Valves don’t work, stay shut
Septation of outflow malformation
pulmonary hypertension
Tetralogy of Fallot
4 abnormalities found in the conus and truncus region
Happens at separation b/w pulmonary trunk and aorta
1. narrow right ventricular outflow region (reduced outflow)
2. defect in interventricular septum
3. Hypertrophied aorta due to pulmonary trunk stenosis (aorta takes more blood than normal due to stenosis, arising cranial to the interventricular defect – “overriding aorta” grows to right side)
4. Hypertrophy of right ventricular wall due to increased pressure on this side, after birth
*can result in blue baby due to mixing of arterial and venous blood
Mesothelioma
mesothelium on surface of lungs
many WBC present due to uncontrolled mitosis in mesothelium
Pericarditis
infection by pathogen cause inflammation of pericardium
chronic infection –> WBCs
M2 macrophages wall off infection – lay down collagen fibers (thick fibrous CT epicardium results)
–thick granulomatous formed
If infection lasts for long time, resident fibroblasts and adipocytes of aerolar CT stimulate growth of collagen and adipocytes
Epicardium now very thick
Similarities of pericarditis and mesothelioma
cellular destruction inflammation chronic -- scar tissue formation epicardium thickened macrophage infiltration
Cardiac tamponade
excessive accumulation of pericardial fluid with pericarditis
expansion of heart is restricted
fluid drained via needle aspiration
Signs and symptoms of cardiac tamponade
Signs:
cardiac output reduced (oxygenation to periph tissues reduced)
inc HR to compensate
inc BP
inc respiration rate to compensate
edema, swelling in ankles, lower legs, abdomen
fever
Symptoms
difficulty breathing when reclining
lightheadedness, dizziness, fatigue
sharp stabbing pain and tightness in chest cavity –> may radiate to left arm/neck
Myocardial infarction
thickening of coronary a walls
occludes delivery of O2 and nutrients to myocardium –> ischemia –> cell death
myocytes die –> cardiac m nonfunctional
series of infarcts (foci of dead cardiac tissue) –> less functional
Histology of myocardial infarct
Day 1
Day 3
Day 10
Day 1: loss of architecture, loss of plasma membrane, disintegration of nuclear membrane, few well-defined nuclei
Day 3: neutrophil inflitration
Day 10: macrophage total removal of necrotic myocytes; myocytes replaced by granulomatous scar tissue
–macro phago dead neutrophils and cardiac myocytes
–transition from M1 –> M2 (TGFbeta and IL-10 –> chemokines recruit fibroblasts to lay down collagen –> granulomatous tissue)
Detectable changes in blood chem in patients with myocardial infarct (isoforms specific to cardiac tissue)
When cardiac myocytes damaged, contents leak out to blood stream
Myoglobin (early)
CK-MB (intermed) – one of the most reliable, early indicators of heart attack
–trauma to skeletal muscle – also release of CK-MB
Troponin I (late – 20-40 hrs after)
Atrioventricular stenosis and aging
calcification of valve and myocardium
reduces blood flow (up to 70-80%)
onset 70-80 yrs
What valve is most affected by calcifications/stenosis with age?
Aortic semilunar valve – lots of pressure in left ventricle to push blood to rest of body
–more scar tissue (collagen) laid down throughout life – calcifies with age
Gestational varicose vv
as fetus gains wt and size, puts pressure on common iliac vv
prevents blood from femoral v to return to heart – blood collects and engorges vv