Pathologies related to the throax: Test 2 Flashcards
what is a multiple myeloma
primary malignant tumor in bone marrow
typically in older
describe spinal metasteses (prevalance, incidence, etiology, etc)
most common tumor in spine
2nd most serious spine pathology
bone = 3rd most common metastasis behind lung and liver
vertebral body, usually anterior, is most common place
spinal metastases are most commonly from what other types of cancers
most often from breast, lung, prostate, kidney, GI, and thyroid tumors
most common region for spinal malignancy
thoracic (70%)
20% create cord compression or myelopathy
risk factors and pathogenesis for spinal malignancy
history of cancer
healthy bone replaced by tumor
clinical manifestations of spinal malignancy
cancer S&S including spine P! that is the most common initial symptom
unfamiliar and severe pain that may become progressive/constant
possibly myeopathy S&S
possible bony alterations including fx or instability
with spinal malignancy, how might bony alterations present
unable to lie flat due to pain
may make the pain mechanical
possibly tender with palpation, percussion and/or vibration at SPs if a spinal fx
PT referral for spinal malignancy
urgent referral unless cord S&S; then you would want to immobilize for an emergency referral
what is thoracic spinal cord myelopathy
slow, gradual and often progressive compression on the cord
incidence of thoracic spinal cord myelopathy
most common region of the spine for myelopathy due to smaller ratio of canal to cord then other regions
etiology of thoracic spinal cord myelopathy
most commonly due to degenerative spinal changes
-lax ligamenyum flavum/buckling
-stenosis
-ARDD with herniation
-vertebral body collapse/fx
-pathological instability
malignancy 20% of the time (red flag = hx cancer)
rare central disc herniation
clinical manifestations for thoracic spinal cord myelopathy
neuro S&S depends on level of injury
extreme spinal P!
multi segment numbers and weakness/paralysis of extremities and trunk below level of injury
spastic/retentive bladder/bowel
hyperactive DTR
+ UMN tests
hypoactive superficial reflexes
immobilize and emergency referral
incidence of non-traumatic spinal fractures
most common serious spinal pathology
70% of non traumatic spinal fx occur in thoracic spine
predominately in older females with osteoporosis
most common between T8 and L4
etiology of non-traumatic spinal fx
malignancy
osteoporosis
risk factors for non traumatic spinal fx
prior osteoporotic or low impact spinal fx
more than 3 months corticosteroid use
female (late onset menarche or early menopause)
older age (women over 65, men over 75)
low evidence for hx of cancer
pathogenesis of non traumatic spinal fx
weakening and eventual failing of bone due to disease
clinical S&S of non traumatic spinal fx
thoracic pain with hx or malignancy or osteoporosis
low evidence for:
-unfamiliar/severe P!
-tender with palpation, percussion, and/or vibration
-sudden change in spine posture/shape
-likely mechanical P!
-rare neuro S&S in LE
preferred imaging for non traumatic spinal fx
x-ray is first choice; lateral views most useful (but they can’t determine age of fracture)
how useful are MRIs for non traumatic spinal fx
can differentiate between osteoporotic and soft tissue malignant fx
can determine age of fracture by identifying bone marrow edema that x-ray cant pick up
should be performed if multiple fractures are found with an x-ray
incidence of spinal infection
uncommon in wealthier countries but resurgence with longevity and IV drug use
in lower income countries more due to HIV/AIDS and TB
skeletal tuberculosis (aka potts disease) is more common in the thoracic spine
etiology of spinal infection
primarily from mycobacterium TB
staphylococcus aureus and brucella are also involved at times
risk factors for spinal infection
imunosuppresion
surgery (particularly of the spine and repeated procedures)
IV drug use
social depravation
Hx of TB
recent infection
pathogenesis of spinal infection
develops 2-3 years after initial air droplet infection into lungs
spreads via lymph and blood
infection starts in lungs (pulmonary TB), goes to vertebral body (osteomyelitis), and eventually the disc (disci tis) and adjacent vertebrae (skeletal TB)
abcess grows
what happens when an abscess grows from a spinal infection
nerve root irritation
vertebral body collapse/fx
cord compression may develop
early S&S of spinal infection
arthritic like back pain/stiffness = most common presenting
constitutional symptoms not common initially
low evidence S&S of spinal infection
localized/progressive pain
infection S&S (especially fatigue, fever since onset of pain, and unexplained weight loss)
tenderness with palpation, percussion and vibration
what happens if spinal infection is left untreated
neuro S&S influence LE coordination as well as bowel/bladder function
increased thoracic kyphosis
what might you see in an x-ray of a pt with spinal infection
body destruction
TB abscess
loss of height
sclerotic end plates
diminished disc space
what are the 2 types of angina
stable = occurring with stress; physical and/or emotional
unstable = occurs at rest
incidence of angina and MI
most often in makes older than 65
risk factors for angina and MI
any condition that limits blood supply to or increases demand of the heart
smoking
metabolic syndromes
-high cholesterol
-HTN
-diabetes
-obesity
-high triglycerides
psychological disorders
SAD
pathophysiology of angina or MI
ischemia or limited circulation with imbalance between supply and demand for the heart with possible complete occlusion and myocardial tissue death
typical manifestations/S&S of angina or MI
Pain (sudden chest pain, pain in jaw/L arm, referred pain)
SOB
Sweating
nausea
fatigue
syncope
atypical manifestations/S&S of angina and MI
females = intrascapular pain, R arm pain, and lack of angina
less pain with diabetes due to neuropathy
pericarditis with autoimmune diseases
most common S&S in older adults is SOB due to impaired ANS response and central P! mechanisms
PT implications for angina and MI
don’t want to miss
for stable angina, if less than 20 min then urgent referral; if more than 20 min then emergency referral
unstable angina = emergency
what is a pulmonary embolism
blockage of the pulmonary artery
incidence of pulmonary embolism
associated with high morbidity/mortality
half go undiagnosed
1/3 pts with untreated die
only 8% of those who are diagnosed die
more common in females over 50
risk factors for pulmonary embolism
prior PE or deep vein thrombosis
immobility
Hx of abdominal/pelvic sx or malignancy
LE joint replacement
late stage pregnancy
LE fx
etiology of pulmonary embolism
most often deep vein thrombosis especially in LE
other blockages may be from fat, air bubbles, amniotic fluid, clumps of parasites, or tumors
pathogenesis of pulmonary embolism
obstruction travels through the right side of the heart abd becomes lodged in smaller pulmonary artery feeding the lungs
pulmonary infection results including damage and impaired gas exchange
clinical manifestations and S&S of pulmonary embolism
often non specific
pleuritic chest pain (sudden sharp/stabbing chest pain) made worse by deep breath, coughing, trunk motion, reaching, and accessory motion testing
SOB, wheezing, and/or rapid breathing
other S&S of pulmonary embolism
cough, possibly with blood
painful breathing
fainting
tachycardia and palpitations
PT implications for pulmonary embolism
don’t want to miss
timely detection is critical
utilize CDR and emergency referral is indicated
PT implications for upper GI system issues
need to differentiate from cardiopulmonary issues
thoughtful positioning with interventions; keep more upright
incidence of gastroesophageal reflux disease
one of the most common digestive disorders, especially in older
2/3 of US adults will experience GERD S&S
etiology of gastroesophageal reflux disease
foods
obesity
smoking
hiatal hernia
medications
pathogenesis of gastroesophageal reflux disease
dysfunctional valve between stomach and esophagus allowing back flow of stomach contents
increased acidity and acid volume
esophagitis - inflammation/injury of esophagus
clinical manifestations and S&S of gastroesophageal reflux disease
heartburn or chest P!/tightness especially after meals, when reclining; may refer to the neck
regurgitation
dysphagia
odynophagia (painful swallowing)
belching
nausea
what is a peptic ulcer
discontinuation of GI track lining
incidence of peptic ulcer
decreasing due to better hygiene and sanitation worldwide
etiology of peptic ulcer
H pyloric bacteria
non steroidal inflammatory drugs (NSAIDs)
pathogenesis of peptic ulcer
imbalance of protective and destructive factors
lining becomes more susceptible to acids
not able to secrete neutralizing bicarbonate
clinical manifestations and S&S of peptic ulcer
check pain, possibly in the mid thoracic or supraclavicular regions (possibly at night; may be temporarily relieved with eating and antacids)
abdominal bloating/fullness
N&V, possibly with blood
weight changes
PT implications of peptic ulcer
usually a urgent referral but emergency if:
progressive dysphagia
persistent vomiting
family history of GI malignancy
what is scheurmann disease (kyphoscoliosis)
anterior vertebral body wedging of adjacent thoracic vertebrae in adolescents
incidence of scheuermann disease
most common cause of adolescent hyperkyphosis
more often in males
etiology of scheuermann disease
possibly inherited but unknown, possible collagen abnormality
medic changed following acute IDD
pathogenesis of scheuermann disease
abnormal vertebral endplate mineralization and ossification during growth that leads ro anterior vertebral wedging and schmorl’s nodes (disc herniated into vertebral body)
clinical manifestations and S&S of scheuermann disease
excessive and rigid thoracic kyphosis that does not change in supine/prone positions
thoracic pain
worse with activity
better with rest
possible counter hyperlordosis in cervical/lumbar regions
what is varicella zoster virus
causes chicken pox (1st occurrence and typically milder) and shingles (2nd occurrence and typically more severe)
mostly an urgent referral but an emergency referral if close to the eye
risk factors for varicella zoster virus
hx of chickenpox is necessary to develop shingles
can develop shingles more than 1 time
increased risk around 50 years of age
significant decline since vaccine was developed
transmission of varicella zoster virus
airborne or direct contact so you should isolate until crusted lesions dry
highly contagious to those who’ve not had chicken pox and 2-3 days prior to symptoms; you won’t get shingles but you will get chicken pox
pathogenesis of varicella zoster virus
travels from lymph through blood and eventually to nerve endings
eventually suppressed but can persist in latency in dorsal root
subsequent infections are triggered with lowered immunity/stress
clinical manifestations and S&S of shingles
shingles skin lesions and paresthesias occur in dermatomal patter (typically T3-L3)
“dewdrop on a rose petal” - vesicle on a red base that erupt
may affect any dorsal root or even a cranial nerve
P! and itching
low risk of developing into postherpetic neuralgia (P! > 90 days after onset)
