Path II Final Flashcards
Three signs of increased intracranial pressure
headache
nausea/vomiting
papilledema
most dangerous cause of increased intracranial pressure
brain tumor
Hydrocephalus Ex Vacuo is due to
brain atrophy disease
more common in elderly
symptoms of Hydrocephalus Ex Vacuo
bent knees
stooped posture
incontinence
loss of memory
With Hydrocephalus Ex Vacuo
loss of neurons or axons in the white matter leaves space in the cranial fossa to be filled with CSF
Is there increased ICP with Hydrocephalus Ex Vacuo
no
Signs of hydrocephalus in a child
Unequal measurements on each hemisphere of the head
Complications of hydrocephalus in a child
increased ICP
cerebellar tonsil herniation
Cerebral vascular disease
aka stroke #3 cause of death in US
3 types of stroke
generalized reduction in blood flow
infarct
hemorrhage
Generalized reduction in blood flow to the brain can be due to
Vascular shock: dramatic decrease in blood flow in the whole body
dilation of blood vessels leads to decrease in blood flow to the brain (gravity)
rare
Brain infarct
aka ischemic stroke
most common cause of stroke
obstruction in blood flow to brain leads to necrosis of tissue due to hypoxia
Brain Hemorrhage
aka hemorrhagic stroke
can be intracerebral or subarachnoid
Lacunar Infarction
aka hyaline arteriosclerosis
more common with advanced hypertension
arteriosclerosis of capillaries leads to microinfarctions
may find absence of motor function
What type of necrosis does the brain undergo?
liquefactive
what are neurons replaced with after a stroke?
microglia
Most common areas of atheroma development
cerebral artery
mesenteric artery
coronary artery
arteries of the extremities
Sources of emboli that may cause stroke:
mitral stenosis
bacterial endocarditis
valve replacement
myocardial infarction
Transient ischemic attack
temporary ischemic stroke
manifests as a true ischemic stroke but is temporary
all brain function is restored afterward
amaurosis fugax
temporary unilateral loss of vision
associated with thrombus in ophthalmic artery
What percentage of people develop full blown stroke within 6 months of TIA
1/3
Intracerebral hemorrhagic stroke
aka parenchymal or hypertensive
develops in people with long term hypertension as a result of hyaline arteriosclerosis
result of long term hypertension in brain
microaneurysm formed in peripheral arteries of the brain ruptures causing pressure on the adjacent vessels
mechanical compression of brain tissue leads to
development of neurological deficit
causes compression of walls of ventricles
promotes non-communicating hydrocephalus
Blood in the brain:
toxic
causes nerve atrophy and necrosis
Subarachnoid Hemorrhagic stroke
aka saccular or berry aneurysm
slow pouching of vascular wall into aneurysm
rupture before 50 years of age
Giant brain aneurysm
1-5cm
signs of brain tumor
not as vulnerable as a berry aneurysm
Traumatic Brain injury
caused by hematoma
30% die as a result
70% live with permanent diability
Epidural hematoma
above dura mater
rupture of the middle meningeal artery
causes separation of the dura from the cranium, compressing the brain
epidural hematoma leads to
pain/neurological deficits
herniation
non-communicating hydrocephalus
Subfalcine herniation
characterized by compression of cingulate gyrus against falx cerebri
can cause compression of anterior cerebral artery
transtentorial herniation
aka uncal/uncinate herniation
much more serious herniation
develops from compression of the free margin of the temporal lobe
complications of transtentorial herniation
compression of parasympathetic fibers of oculomotor- pupil dilation on involved side
compression of posterior cerebral artery
cerebellar herniation
aka tonsilar herniation
most dangerous herniation
like an acute arnold-chiari malformation
cerebellar herniation results in
compression of the brainstem (cardiac and respiratory centers)
leading to immediate death
Duret Hemorrhage
aka secondary brainstem herniation
hemorrhage into the pons
assocaited with cerebellar herniation
due to kink in basilar artery
Subdural hematoma
rupture of bridging vein
blood flows into subarachnoid space
see the same type of manifestations as epidural hematoma but not as acute
creates lake on cerebral surface leading to poisoning of grey matter
causes of subdural hematoma
sudden change in speed of head movement
shift can tear veins
Traumatic parenchymal brain injury
damage to brain parenchyme
categories of Traumatic parenchymal brain injury
Concussion
Contusion
Laceration
Basilar skull fx
Concussion
characterized by immediate and transient loss of neurological function secondary to mechanicl forces
2 major manifestations of concussion
loss of consciousness
retrograde amnesia
Loss of consciousness (concussion)
can be short or long term
functional loss of reticular formation
neurons that have contact with different parts of the brain are disrupted
loss of consciousness has to do with the time needed for restoration of contacts
retrograde amnesia (concussion)
permanent loss of memory about events immediately before/after and during the trauma
completely erased from memory
Contusion
hemorrhage into the superficial layers of the brain
due to blunt trauma
types of brain contusion
Coup: damage is at impact site, head immoble/force mobile
Contre-coup: damage opposite the impact sire, head mobile/force immoble
Laceration of brain tissue
real tear in tissue, never comes back
associated with tear in blood vessels
basilar skull fracture
very brittle/thin
predisposes to infection in CNS
Signs of basilar skull fx
Rinorhea- CSF leakage from nose, bilateral periorbital bruising
Otorhea- CSF leakage from ear, battle sign
Rheumatoid arthritis
chronic inflammatory autoimune disease
age at RA onset
40’s-50’s
Pathogenesis of RA
attacks synovium, hyperplasia takes synovium from 1-4 cell layers to over 400
pannus formation in joints (granulation-like tissue)
loss of articular cartilage with pariarticular bone loss
RA symptoms
acculumation of exudate in joints
ulnar deviation of the fingers
atrophy of lumbricals and interossei
tenosynovitis
periarticular osteopenia
seen with RA
inflammation near bone leads to loss of local bone density
long term inflammation leads to cytokine release, stimulating osteoclasts to resorb bone resulting in erosions
Swan Neck deformity
hyperextension of the PIP
hyperflexion of the DIP
Boutonniere deformity
hyperflexion of the PIP
hyperextension of the DIP
Effect of RA on the feet
contracture leads to hammer toes
bunion on outside of 1st MTP due to hallux valgus
callus on bottom of feet due to hyperplasia
loss of arch
effect of RA on the knee
swelling in knee joint
exercise will injure the joint (fluid is incompressible so will damage bones)
effect of RA on hip
compression of vessels and nerve leads to destruction of femur head
corticosteroid injection will cause aseptic osteonecrosis
protrusio acetabuli
Rheumatoid nodule
sign of disease progression into more severe involvment
involvement of blood vessels- vasculitis
can be anywhere and have many different characteristics, commonly seen on elbow
Kaplan’s syndrome
rheumatoid arthritis and interstitial fibrosis in lung
Juveline Rheumatoid Arthritis
presenting in patients under 16
usually seronegative
Specific features in juvenile RA
Knee jt involvement- arthritic leg grows longer receding chin still's disease extensive multiple deformations fixed FHP neutropenia increased ADI
Still’s Disease
hepatosplenomegaly
lymphadenopathy
fever
Felty’s syndrome
neutropenia- low concentration of neutrophils in blood, also see leukopenia
body is prone to infection
Osteoarthritis
non-inflammatory
most common degenerative joint diseae
Primary target of OA
cartilage
Primary OA
unknown cause
secondary OA
known cause
more predictable
Heberden’s node
irregular hyperplastic bony nodule
DIP
Bouchard’s node
PIP
periarticular osteosclerosis
increased density of endplate in OA
OA in the knee
will see narrowing of the medial portion of the jt space causing bowing of the legs
osteophyte formation
OA in the hip
can be crippling
will change posture/gait
degenerative changes in acetabulum and on femoral head
Spinal involvement in OA
decreased IVD height
osteophytes on margins
decrease in IVF diameter
Slippage of the facet joint
Bronchi
covered by cartilage
have goblet cells producing mucous
submucosal mucous glands
Bronchioles
no cartilage cover
few goblet cells/very little mucous production
diffuse pulmonary disease
involves both lungs
two categories:
COPD and restrictive disease
COPD
airway disease
limitation of airflow resulting from an increase in resistance
characterized by normal or increased total lung capacity
types of COPD
bronchial asthma
emphysema
chronic bronchitis
bronchiectasis
Restrictive disease
reduced expansion of lung parenchyma
decreased total lung capacity
Bronchial asthma
episodic, reversible
exaggerated bronchospasm due to various stimuli
Extrinsic asthma
aka atopic asthma
initiated by a type I hypersensitivity reaction (anaphylaxis)
induced by reaction to extrinsic antigen (ie pollen)
Pathogenesis of extrinsic asthma
first exposure to antigen- type I immune response,
IgE immunoglobulin located on mast cell
prepares for next encounter
Second exposure to antigen- formation of immune complex leading to mast cell degranulation and asthmatic attack
4 major phenomena in extrinsic asthma
vasodilation
increased permeability of blood vessels
bronchospasm
increased mucous production
Functions of histamine in extrinsic asthma
causes increased blood vessel permability (lumen swelling) causes vasodilation (more blood flow, increased swelling, lumen narrowing) stimulates mucous production (further airway obstruction)
Histamine stimulation of vagus nerve
through the ganglia- return of stimulation through parasympathetic fibers resulting in nerve dysfunction and bronchospasm
Charcot Leyden crystals
pathomnemonic sign of bronchial asthma
rhomboid shaped crystal found in sputum
made of protein released after destruction of eosinophils
Status asthmaticus
severe asthmatic attack lasts for days to weeks
may result in death
Bronchial asthma characterized by 3 major clinical factors
expirational dyspnea (shortness of breath due to inability to remove air from lungs)
cough (expectorates mucous)
wheezing (narrowing of lumen causes whistling sound)
Intrinsic asthma
aka non-atopic
same manifestations of extrinsic, however triggering mechanisms are non-immune
Pathogenesis of intrinsic asthma
pulmonary or bronchial infection most common provoker (virus)
can also be due to some drugs, psychological stress, atlas misalignment
Emphysema
characterized my permanent enlargement of airspaces distal to terminal bronchioles accompanied by alveolar wall destruction
irreversible
Terminal bronchioles
less than 2mm
aka acinus or primary respiratory unit
consists of respiratory bronchiole, small alveolar duct, alveoli
Consequences of alveolar tear
results in dramatic decrease in blood flow
blood pools in the lungs causing hypertrophy of the right ventricle and less blood flow to left ventricle causing less oxygenation of the body
3 types of emphysema
Centracinar
panacinar
distal acinar
Centracinar emphysema
AKA centrilobular proximal acini affected while distal alveoli are spared only respiratory bronchioles distended alveoli and alveolar ducts not involved usually develops in upper lobes of lungs
Panacinar emphysema
all components of acini are involved/ uniformly enlarged
occurs in lower lobes of the lungs
Distal acinar emphysema
aka paraseptal emphysema
distal acini are affected while proximal are spared
usually develops in upper lung lobes
common cause of spontaneous pneumothorax
Protease-antiprotease theory
AKA oxidase-antioxidase theory
with lung infection- neutrophils release elastase to attack infection and antielastase prevents excess lung damage
Deceased levels of antielastase in lungs of those with emphysema
Chronic Bronchitis
caused by inhaled irritants,, decreases resistance of bronchial wall to infection
results in inflammation, hyperplasia of goblet cells, and then metaplasia to replace goblet cells with squamous cells
Bronchiolitis obliterans
aka small airway disease
occurs after metaplasia in lungs to replace goblet cells with squamous cells
lack of normal gas exchange leads to inflammation causing bronchiole wall fibrosis and irreversible narrowing of the lumen
Chronic bronchitis and Bronchiolitis obliterans predisposes to
lung cancer
chronic infection- lack of normal cells with villi to remove debris
Bronchiectasis
characterized by permanent dilation of bronchi and bronchioles
caused by destruction of muscle and elastic tissue
results in chronic necrotizing infections
Predisposing conditions to Bronchiectasis
Kartagener syndrome- lack of alveoli vili movement, infection flourishes
Kartagener syndrome
genetic disease
lack of mobility in sperm and alveolar villi
Restrictive pulmonary disease
Reduced total lung capacity
extrapulmonary or intrapulmonary origin
Extrapulmonary origin of Restrictive pulmonary disease
obesity
kyphoscoliosis (pott’s disease)
restricted ROM
high placement of diaphragm
intrapulmonary origin of Restrictive pulmonary disease
acute
chronic interstitial lung disease ie:
scleroderma (systemic sclerosis of lung)
overactivity of fibroblasts
replacement of lung tissue with scar tissue
lung shrinkage resulting in contractive atelectasis
Hamman-Rich syndrome
idiopathic pulmonary fibrosis
honeycomb appearance to lungs
Sarcoidosis
most common granulomatous non-caseating disease
characterized by hilus lymphadenopathy
involves eyes and skin
Pneumoconiosis
Development of lung fibrosis due to dust exposure
different names depending on type of dust
silicosis=silica
asbestosis=asbestos
anthracosis=coal dust (aka coal worker’s pneumoconiosis)
Most dangerous part of cigarette
paper- produces 1200 carcinogens while burning
Lung Cancer
aka bronchiogenic carcinomas
95% of lung tumors are due to lung cancer
common features of bronchiogenic carcinoma
majority arise in epithelium of major bronchi near hilus
associated with smoking
aggressive, locally invasive, widely metastisizing neoplasm
all have capacity to make bioactive products producing paraneoplasmic syndromes
80% of inappropriate ADH secretion is due to
lung cancer
Squamous cell carcinoma
25-40% of lung cancers
most common
least malignant
more common in males
Small cell carcinoma
20-25% of lung cancers
most malignant
aka oat cell carcinoma
6 months to live after dx
Adenocarcinoma
25-40%
multiple subtypes (acinar, papillary, bronchioloalveolar, solid, mixed)
have a peripheral location (can be removed if caught in time)
most common lung cancer in women
Large cell carcinoma
10-15%
large cell neuroendocrine carcinoma
rare but very aggressive, mets to lymph nodes in trachea
Pancoast tumor
aka apical tumor
no histological pattern
develops unilaterally
destroys C7, T1, and first rib, may extend out as well
compresses brachial plexus, characterized by spinal pain
Virchow’s nodes
seen with pancoast tumors
lymphadenopathy of supraclavicular lymph nodes with lung cancer or stomach cancer
Horner’s syndrome
develops with pancoast tumors anhydrosis- lack of sweating ptosis- drooping of eyelid meiosis- narrowing of pupil anophthalmus- eyeball sunk into orbit
Mesothelioma
tumor resulting from exposure to asbestos
100x higher chance of developing in smokers
Cannonball metastasis
seen with osteosarcoma
