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Final Exam

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1
Describe angina at rest
prolonged (>20 minutes)
NSTEMI presentation
2
Describe new onset angina
new angina that limits activity
brought on by walking or climbing stairs
3
Describe increasing angina
previously diagnosed angina that is now different
longer in duration
more frequent
lower threshold of activity
4
Angina can be induced by
exercise
stress
cold weather
5
SX of angina is usually lesss than ____ minutes and up to ____ minutes
10
20
6
How does angina resolve?
within 2-5 after rest or with nitroglycerin
7
How does chest pain present with an AMI?
prolonged and more severe
n/v
SOB
diaphoresis
no response to SL NTG
8
How will a NSTEMI present on EKG and lab work?
abnormal biomarkers
EKG changes that do not meet STEMI criteria
9
when should you repeat troponin?
after 3 hours
10
What is used to determine the heart score?
history
ECG
age
risk factors
troponin
11
A heart score greater than or equal to 4
require further investigation
12
Treatment with PCI is for
persisten sx
STEMI
13
What are the main stay drugs for NSTEMI?
antiplatelet
antithrombin
nitrates
14
Early invasive approach as with STEMI if
refractory angina
hemodynamic or electrophysiologic instability
increased risk
15
invasive therapy is recommended with 24 hours if
recurrent angina w/ or w/out
sx of CHF
elevated troponin
new ST segment depression
16
When should an early invasive approach occur within 2 hours?
patient has unstable angina and hemodynamically unstable
17
How should ASA be given and for what?
325 mg on arrival or before
unstable angina, STEMI, NSTEMI
18
What are the absolute CI with ASA?
active PUD
allergy
19
What is an alterantive to ASA?
clopidogrel
20
If a CABG is schedule when should you stop copidogrel?
withhold for 5 days prior
21
Do you need to stop clopidogrel for PCI?
no
22
How do nitrates work?
relax smooth muscle in arteries/arterioles and veins
reduce pul capillary wedge pressure/systemic arterial pressures
decreases LV end diastolic and systolic pressures
reduce RV and LV filing pressures
23
When is IV NTG recommended for the first 24-48 hours?
STEMI
recurrent ischemia
CHF
HTN
24
Which type of ischemia should you be catious in using NTG with?
inferior wall
25
How long do you have to wait to give NTG to patients who have recently taking sildenafil or tadalafil?
24 hours for sildenafil
48 hours for tadalafil
26
What is the most common site of peripheral artery disease?
femoral and popliteal
27
What is the most common symptom of PAD?
intermittent claudication
28
What are some other s/s of PAD?
pain at rest
asymptomatic
29
What are some physical findings of pad?
decreased or absent pulses distal to obstruction
presence of bruit over the narrowed artery
impotence is a sign of iliac disease
30
What are some sign of severe PAD?
decreased hair growth on legs
smooth and shiny skin
cool temp of foot and leg
paleness of the leg or foot when elevated
blue or red discoloration of the foot when hanging down
sore on foot that does not heal
31
What is used to calculate PAD?
ABI (ankle brachial index)
32
What are the the 5 ps of acute arterial occlusion?
pain
paresthesias
pallor or cyanosis
paralysis
pulselessness-coolness
33
What is used to view acute limb ischemia?
doppler
34
What is the treatmen for acute limb ischemia?
immediate revascularization
anticoagulation with IV heparin
35
When limb viability is jeapardized in acute limb ischemia what must be done?
catheter directed thrombolysis/thrombectomy
surgical thromboembolectomy and arterial bypass
36
What is the test for thoracic outlet syndrome?
Adson's maneuver
37
What is involved in the ischemic phase of raynauds phenomenon?
blanching/cyanosis
cold sensation
paresthesia
38
What is involved in the rewarming phase of raynauds phenomenon?
reactive hyperemia
throbbing pain
39
What is the modality of choice to demonstrate the anatomy and size of a thoracic aneurysm?
CT
40
What imaging can diagnose a thoracic aortic aneurysm?
chest x ray
41
What are the s/s of thoracic aortic aneurysm?
substernal back or neck pain
asymptomatic
42
Presure on the trachea, esophagus or superior vena cava from a TAA can cause?
dyspnea
stridor
cough
dysphagia
43
Most abdominal aortic aneursyms are
asymptomatic until rupture
44
What are the commonly preceding s/s of AAA rupture?
back or abdominal pain
hypotension
palpable abdominal mass
45
Most aneursym are found ____?
incidentally on US or CT
46
What is the study of choice for screening for a AAA?
US
47
What is the study of choice for reliable assessment of an AAA? when should it be done?
CT
when the diameter nears 5.5 cm
48
If a patient has an AAA that is less than 4 cm how often with they need to follow up with US?
every 2 years
49
When an AAA starts approaching 5 cm how often should they follow up with US?
every 6 months
50
Who should be screened for an AAA?
65-75 year old men who are current or past smokers
51
What may indicated impending rupture of an AAA?
pain or tenderness
52
What are some s/s of varicose veins?
dull aching heaviness or feeling fatigue after standing
dilated totuous veins of the thigh/calf are visible and palpable when the patient is standing
53
How should you examine a patient with varicose veins?
supine and standing
54
What are some finding of deep venous insuffieciency?
increased leg circumference
venous varicosities
edema
skin changes
55
Venous stasis may produce
hyperpigmentation
erythema
eczema
56
What is a test used to examine varicose veins?
trendelenburg test
57
How is the trendelenburg test done?
patient supine with leg elevated
tourniquet placed on the proximal part of the thigh
patient is asked to stand
58
Filling of the varicose veins within 30 seconds indicates the varicose veins are caused by what?
deep enous insufficiency and incompetent perforating veins
59
If venous refilling occurs promptly after tourniquet removal there is an insufficiency in which veins?
superficial
60
What imaging can be done for varicose veins?
doppler/duplex US
61
What can be done to manage varicose veins?
leg elevation
regular exercise
TED stockings
laser treatment
vein ligation and stripping
sclerotherapy
62
What does sclerotherapy do?
infection of sclerosing agent induces permanent fibrosis and obliteration of the target veins
63
What are some complication of varicose veins?
phlebitis
tissue necrosis
infection
64
What are some risk factors for venous insufficiency?
age
hereditary
pregnancy
standing occupation
obesity
prior injury or surgery
sedentary lifestyle
65
What are the symptoms of venous insufficiency?
leg pain, aching or cramping
burning or itching of the skin
leg or ankle swelling
heavy feeling in legs
skin discoloration or texture changes
restless legs
66
T/F symptoms of venous insufficiency are correlated with the number and size of varicosities?
false
67
What are some symptoms of venous disease symptoms?
aching, heaviness discomfort in the calf of the affected limb
particularly worse at the end of the day
symptoms reduced in the morning
68
What are the most common sites of a venous ulcer?
medial aspect of ankle
lower 1/3 of leg
69
What are the characteristic features of a venous ulcer?
superficial
painless
irregular
ragged
sloping edges
pink base, unhealthy granulations
70
T/F venous ulcers penetrate into the deep fascia?
false they never do
71
Venous ulcers are complications of?
chronic venous insufficiency
72
Nonsurgical management for CVI?
graduated compression stockings
unna's boots- paste gauze boots
multilayer elastic wraps or dressings
pneumatic compression devices
73
What should you educated your patient on with managing CVI?
avoid prolonged sitting or standing
frequent leg elevation
74
What are the type of venous thromboembolism?
superficial
deep
75
Where is the most common site of a DVT?
calf
76
What is virchows triad?
stasis
venous wall injury
hypercoagulability
77
What can create a hypercoagulable state?
post op
cancer
thrombophilia
estrogen therapy
pregnancy
postpartum period
IBD
78
What can create endothelial injury
surgery
trauma
indwelling cath
atherosclerosis
heart valve disease or replacement
79
What can cause venous stasis?
immobility
paralysis
heart faiulre
venous insufficiency
80
What are the clinical manifestation of a DVT?
pain
edema
increased cirumference
positive homan's sign
81
What are some signs of a superficial DVT?
erythema
warm
tenderness
82
What is homans sign?
dorsiflexion of the foot produces calf pain
83
When should you not check homan's sign?
if you already know a DVT is present
84
How do you manage a DVT?
elastic stocking or bandage
anticoagulatants
warm moist heat
85
What are some anticoagulants used to treat a DVT?
IV heparin
NOAC (coumadin)
86
What are the primary causes of lyphedema?
congenital
87
What are the secondary causes of lymphedema?
axillary node dissection
radiation therapy
trauma
infection
malignancy
88
What is the most common form of pericarditis?
acute
89
What are the forms of acute pericarditis?
firbinous vs effusive
90
How long does pericarditis last?
less than 6 weeks
91
What are the types of subacute pericarditis?
effusive and constrictive
92
How long does subacute pericarditis last?
6 weeks to 6 months
93
What are the types of chronic pericarditis?
constrictive and adhesive
94
What are some clinical findings of acute pericarditis?
chest pain that can be severe
referred pain to the neck, arm and left shoulder
pain worsened by inspiration or caughing
pain worse when lying supine and relieved by leaning forward
pericardial fruction rub
EKG changes
95
What do you see on stage 1 on an EKG of acute pericarditis?
widespread ST segment elevation with upward concavity in leads 2,3, V2-V6 with reciprocal dpression in aVR
96
what is the treatment for acute pericarditis?
bed rest
NSAIDs
omeprazole (to protect gastric mucosa from NSAID)
colchicine
97
When do you give a patient with acute pericarditis glucocorticoid?
if failed treatment or intolerance to NSAIDs
98
What is the dosing for colchicine? When is it contraindicated?
less than 70 kg - 0.5 mg QD
greater than 70 kg- 0.5 mg BID
patients with hepatic or renal dysfunction
99
What are the two types of NSAIDs you can use to treat acute pericarditis?
ibuprofen 800 mg TID
indomethacin 225 mg TID
100
What is a compication of pericardial effucion?
cardiac tamponade
101
What is becks triad/
hypotension
soft/absent/muffled heart sounds
JVD
102
rapid progression of cardiac tamponade can occur with ___ ml
200
103
slow progression of cardiac tamponade can occur with > __ L
2
104
How do you diagnose a pericardial effusion?
echocardiogram
105
Is echocardiogram specific or sensitive for pericardial effusion?
both
106
What is the treatment for pericardial effusion?
pericardiocentesis
107
What are the three approaches for a pericardiocentesis?
subxyphoid
apical
parasternal
108
What causes endocarditis?
bacterial or fungal infection inolving the valves and or endocardial surface tissue
109
clinical presentation for endocarditis depends on?
valves involved
virulence of organism
110
What is the most common bacterial etiology of endocarditis?
staph aureus
111
The oral cavitiiy is a portal for which organisms?
viridans streptococci
staphylococci
heamophilus
aggregatibacter
cardiobacterium hominus
eikenella corrodens
kingella kingae
112
What are the risk factors for endocarditis?
old age
artifical valves
damages valves
congenital heart defects
PWID
poor dental health
long term cath palcement
113
What are the clinical findings for endocarditis?
fever
petechiae on palate, conjuctiva, subungual tissue
osler nodes (toes, fingers, feet- painful)
janeway lesions (palms and soles- painless)
murmur
114
What lab findings with you find with endocarditis?
hematuria
protinueira
115
How is endocarditis diagnosed?
blood culture
three two bottle sets from different sites over two hour time frame
116
What imaging is done for endocarditis?
echocardiogram
117
What is the common age of onset for primary essential HTN?
25-50
118
What can cause primary esential HTN?
sypathetic nervous system hypersensitivity
abnormal CV or renal development
renin-angiotensin system activity
defect in natriuresis
intracellular Na+ and Ca+
119
What are the complication of untreated HTN?
hypertensive CVA
dementia
hypertensive renal dz
aortic dissections
atherosclerosis
120
What are the criteria for metabolic syndrome?
must have 3 or more:
abdominal obesity
blood pressure > 130/85
low HDL
triglycerids over 150
fasting glucose over 100
121
What are some risk factors for developing metabolic syndrome?
sedentary lifestyle
genetics
age older than 60
122
What is the pathophysiology of metabolic syndrome?
free fatty acids release excess fat from tissue causing the hepatic tissue to respond with increased glucose, triglycerides and VLDL
Free fatty acids inhibit insulin mediated glucose upate in muscle cells
123
What is insulin resistance?
decreased ability of insulin to transport glucose into target tissue which causes increased VLDL and decreased HDL
124
How does the body respond to decreased activity of insulin?
impaired supression of glucose production in the liver
impaired tissue uptake of glucose
125
What is the most common liver disease?
non-alcoholic fatty liver disease
126
How does non-alcoholic fatty liver disease happen?
increased FFA causes decreased hepatic fatty acid aoxidation leading to cellular inflammation and oxidative stress
127
What is the pathophysiology of hyperuricema?
hyperinsulinemia causes increased reabsorption of uric acid at renal tubules leading to damage or enal endothelial tissue
128
Is damage from acute hyperuricemia reversible?
yes
129
Is diabetic nephropathy reversable?
no
130
What is the relationship between PCOD and metabolic syndrome?
women with PCOD have insulin resistance and are more likely to develop metabolic syndrome
131
What are the indications for itubation?
respiratory failure
apnea
reduced level of consciousness (GCS <8)
rapid decline in mental status
airway injury or impedning airway compromise
high risk for aspiration
132
What are the respiratory danger signs?
significant work of breathing
stridor/drooling
cyanosis
agonal respirations
133
What are the signs of pancoast's syndrome?
severe pain in the shoulder region
atrophy of hand and arm muscles
horner syndrome (ptosis, miosis)
laryngeal nerve compression (hoarse voice and cough)
134
What does pancoast's syndrome involve anatomically?
brachial plexus
cervical sympathetic nerves
135
What is the most common type of lung cancer seen in non-smokers?
NSCLC- adenocarcinoma
136
How does adenocarcinoma present?
unresolving pneumonia
peripheral nodules/mass
137
which type of cancer is more aggressive?
small cell carcinoma
138
Which cancer does not respond to chemo or resection?
squamous cell carcinoma
139
Which type of cancer has slower spread?
non- small cell lung cancer
140
What is the medial survival rate of small cell carcinoma?
6-18 weeks
141
What is a solitary pulmonary nodule?
coin lesion
<3 cm (isolated, surrounded by normal lung, no associated with infiltrate, atelectasis, adenopathy)
142
Cor Pulmonale involves systolic and diastolic failure of which chamber of the heart?
right ventricle
143
What is Cor Pulmonale most commonly caused by?
pulmonary hypertension
144
Pulmonary hypertension is defined by a mean pulmonary arterial pressure > than?
20 mmHg
145
The WHO classifies group 2 as pulmonary venous HTN caused by?
left sided heart disease
146
WHO classifies group 3 patients as pulmonary HTN due to?
lung disease
147
WHO classifies group 4 patient patients as pulmonary HTN due to?
obstruction
148
What is the gold standard for diagnosing pulmonary hypertension?
right sided cardiac cath
149
What is a VQ scan good for when looking at pulmonary HTN?
helps exculde other causes in advance of diagnosing idiopathic pulmonary HTN
150
What should you do if VQ scan is abnormal?
CT-PA (pulmonary angiography)
151
What causes increase in BNP?
right ventricular stretching
152
Reduced filling of what ventricular causes reduced distensibility and decreases CO causing death?
left ventricle
153
What causes the release of troponin?
myocardial oxygenation decreases
154
What does the right coronary artery supply?
right ventricle
right atrium
SA node
AV node
155
D-dimer is elevated by which process?
breakdown of fibrin
156
What are the hallmark signs for PE?
dyspnea
syncope
hypotension
cyanosis
157
What is the classic finding of a PE?
prominent S wave in lead I
prominent Q wave in lead III
inverted T wave in lead III
158
Is the classic S1, Q3, T3 sensitive or specific?
specific
159
What is the imaging for choice for DVT?
US
160
What is the gold standard for a PE?
chest CT with IV contrast
161
What should be done in a pregnant patient with a possible PE?
VQ scan
162
What is the most common form of ILD of unknown cause?
idiopathic pulmonary fibrosis
163
Which gender is more likely to have idiopathic pulmonary fibrosis?
men
164
What are common hx finding with idiopathic pulmonary fibrosis?
hx of smoking
hx of environmental exposure
165
What is the cause (s) of pleural effusion?
excess fluid production
decreased absorption
166
What is a common presenation of patients with large pleural effusions?
dyspnea
167
What are the PE findings of pleural effusion?
dullness to percussion
decreased breath sounds over the effusion
168
What criteria is used for determining if a fluid is exudative?
lights criteria
169
What is the lights criteria that defines fluid as exudate?
If any of the following are found:
pleural fluid:serum protein >0.5
pleural fluid:serum LDH >0.6
pleural fluid LDH > 2/3rd of the upper limits of normal serum LDH
170
Tall, thin boys/men aged 10-30 years old commonly suffer from what type of pneumothorax? What is their chance of recurrence?
primary spontaneous
50%
171
What causes traumatic pneumothorax?
penetrating and nonpenetrating trauma
172
What causes iatrogenic pneumothorax?
transthoracic needle aspiration
thoracentesis
insertion of central IV catheters
173
A tension pneumothorax occurs with what?
mechanical ventilation
resuscitative efforts
174
How does a patient present with a tension pneumo?
difficulty with ventilation
175
How is a tension pneumo treated?
large bore needle inserted into the pleural space (thoracostamy)
176
In a tension pneumo which way does the mediastinum shift?
away from the affected side
177
What are the triggers for asthma?
exercise
viral URI
inhale allergens
178
What are the rare triggers for asthma?
ASA
food
179
What are the common inhaled allergens that trigger asthma?
mold
dust mites
animal dander
cockroach dander
pollens
180
What is used to treat acute asthma exacerbation?
SABA
systemic glucocorticoid
181
What is given in the ER for acute asthma exacerbation?
IV methylprednisolone
182
COPD patients with emphysema often present with?
dyspnea
183
What do COPD patients with chronic bronchitis often present with?
chronic cough
mucopurulent sputum
chest infections
184
Do COPD patients with emphysema or chronic bronchitis present earlier in age?
chronic bronchitis in 30s/40s
185
What is found on PE with emphysema patients?
accessory muscle use
decreased breathe sounds
pursed lips
barrel-shaped chest
186
What is found on PE with chronic bronchitis patieents?
overweight
cyanotic
peripheral edema
chest noisy with rhonic and wheezing
chronic hypoxia
187
What does a chest x ray show of a patient with chronic bronchitis?
increased bronchial markings
enlarged right heart border
188
What are seen on chest x ray with emphysema?
flattened diaphram
diminished lung markings
hyperinflation
possible blebs
189
What is the most comon viral cause of severe lower respiratory tract illness in the elderly and in children?
respiratory syncytial virus
190
What is the treatment for upper respiratory infection treatment?
rest/fluids
decongestants or saline nasal sprays
anti-inflammatory
191
Which drug leads to rhinitis medicamentosa?
oxymetazoline or phenylephrine
192
What is the treatment for rhinitis medicamentosa?
cessation of sprays
topical intranasal corticosteroids- flunesolide 2 sprays BID
intranasal anticholinergic
short tapering course of oral prednisone
193
What intranasal anticholinergic can you give for rhinits medicamentosa?
ipratropium 0.06% nasal spray, 2-3 sprays every 8 hours prn
194
What is the centor criteria?
used to determine the likely hood of GABHS
195
Whats the criteria for GABHS?
fever over 38
tender anterior cervical adenpathy
lack of cough
pharyngotonsillar exudate

all are present strongly suggests GABHS
2 or 3 is intermediate likelihood
only 1 pressent it is unlikely GABHS
196
Marked lymphadenopathy and white purple tonsillar exudate suggests?
mononucleosis
197
What should be avoided if a patient has mononucleosis?
ampicillin
198
What are the common pathogens of GABHS?
neisseria gonorrhoeae
mycoplasm
chlamydia trachomatis
199
Lack of exudate and rhinorrhea is suggestive of?
virus
200
An infection that penetrates the tonsillar capsule and involves the surrounding tissues
peritonsillar abscess
201
What can a patient with peritonsillar abscess present with ?
severe sore throat
odynophagia
trismus
displaced uvula
"hot potato" voice
202
How is a peritonsillar abscess treated?
amoxicillin 1 gm or 3 gm
clindamycin 600-900 mg
203
When does bronchitis typical start? and with what sx?
1-2 days after URI with gradual onset of cough
204
What are the common viral causes of bronchitis?
influenza A and B
rhinovirus
RSV
coronavirus
adenovirus
205
What are the common bacterial causes of bronchitis?
H. influenzae
S. pneumoniae
206
How long does bronchitis last? How long does the cough last?
7-10 days
6-8 weeks
207
What are the environmental risk factors for screening?
asbestos
benzene
arsenic
formaldehyde
radon
208
What are the common cancer screenings?
mammogram
pap smears
colonoscopy (age 45)
CT scan for smokers with 30 pack year history
PSA/digital rectal exam (50)
skin check
209
What is staging and the three divisions?
classify based on the extent in the body
T, N, M
210
What is important about staging?
common language of communication
guides treatment
estimates prognosis
allows comparison of results
standardizes clinical trials
211
What is cancer grade and how is it used?
classified the cancer cells themselves based on their degree of differentiation and their growth rate
how aggressive they are
usually graded I-IV
212
What occurs when cells within a tissue multiply faster than normal and extra cels build up?
hyperplasia
213
When cells start to look abnormal and there are changes in how the tissue is organized (more advanced than hyperplasia)
dysphagia
214
Abnormal cells that cool like cancer cells grow in a place and do not spread to nearby tissue
carcinoma in situ
215
What is superior vena cava syndrome?
obstruction of blood flow through the SVC
216
What is the most common cause of SVC?
malignancy and extrinsic compression
217
What is the most common type of cancer that will cause extrinsic compression of the SVC?
lung
218
What has lessened the frequency and severity of hypercalcemia in cancer patients?
bisphonates
219
What are the common cancers that caused hypercalcemia?
breast
kidney
lung
prostate
head
neck
multiple myeloma
220
A cancer patient presents with lower limb weakness, heperreflexia and low of bowel or bladder, what is the diagnosis?
spinal cord suppresion
221
What is the treatment for spinal cord compression?
high dose steroids
neurosurgical eval
urgent radiation
possible chemo
222
What is tumor lysis syndrome?
rapid cell breakdown after chemotherapy
223
What is tumor lysis syndrome most common with?
lymphomas
leukemia
224
What is the pathophys behind tumor lysis syndrome?
cells breakdown releasing potassium, phosphate and uric acid causing metabolic changes
225
How can a patient present with lymphoma?
painless lymphadenopathy
fever
weight loss
anorexia
night sweats
malaise
pruritis
pain
airway compression
SVC syndrome
intussusception
226
What will you check on PE with lymphadenopathy
lymph node chains
tonsils
abdominal exam
neurological exam
symptoms of obstruction
227
Which age groups is hodgkins disease typically seen?
15-20s
older than 55
228
Which gender is hodgkins more common in?
male
229
What is related to hodgkins disease?
epstein barr virus
HIV and HTLV1 virus
organ transplants
230
What is a sign of hodkins disease?
reed sternberg cell
231
What is reed sternberg?
abnormal type of B cell
multi-nucleated giant cell
232
What are the B symptoms for hodgkins disease?
fever
night sweats
weight loss (10% or more in last 6 months)
233
B cells represent what for hodgkins disease?
poorer prognosis
234
What other factors represent poorer prognosis for hodgkins disease?
over 45
bulk disease
poor response to therapy
235
What are the two big treatments with hodgkins disease?
bone marrow transplant
immunotherapy
236
T/F hodgkins has a survival rate of 86% and that rate is even higher with children
true
237
T/F hodgkins disease is associated with long periods of remission
true
238
Nonhodkins lymphoma starts in ?
lymph nodes
spleen
bone marrow
239
T/F non hodgkins lymphoma has a wide variation in growth, progression and response to therapy
true
240
What are the common s/s of nonhodgkins lymphoma?
enlarged lymph nodes
chills
weight loss
fatigue
SOB
cough
easy bruising/ bleeding
abdominal swelling or early satiety
chest pain or pressure
severe or frequent infections
241
Where is there poorer prognosis with nonhodkins lymphoma?
bone marrow involvement
large mass
high LDL
CNS disease
testicular involvement
mediastinal involvement
poor response to therapy
242
What can cause leukemia?
radiation
drugs
genetic
viral or immunological factors
243
What are the 2 major disorders of the cells?
unregulated proliferation or failure of apoptosis
incomplete maturation
244
What are the acute leukemias?
AML (acute myelogenous leukemia)
ALL (acute lymphocytic leukemia)
245
What are the chronic leukemias?
CML (chronic myelogenous leukemia)
CLL (chronic lymphocitic leukemia)
246
abrupt onset and progression related to bone marrow failure and invasion of leukemia cells into tissue is classified as acute or chronic leukemia?
acute
247
What are symptoms related to with leukemia?
infiltration of tissues by leukemia cells and crowding out of normal cells
248
What are the s/s of leukemia?
anemia (normocytic, normochromic)
thrombocytopenia
neutropenia
lymphadenopathy
hepatosplenomegaly
testicular enlargement
bone pain
skin infiltration
249
What is the most common childhood leukemia?
ALL
250
What are the subtypes?
T cell and B cell
251
If adults get ALL is their prognosis good or poor?
poor
252
What will you see on slides that is indicicative of AML?
auer rods
253
Who has a better prognosis with AML?
adults over kids
254
Patient with chronic leukemia may be ___ for months or years?
asymptomatic
255
What are the phases of chronic leukemia?
indolent
agressive
256
Chronic leukemias are uncommon in what population?
children
257
Which leukemia is associated with the philadelphia chromosome?
chronic myelogenous leukemia
258
What additional phase does CML have?
blast crisis
259
What is the treatment for CML?
bone marrow transfusion
260
Tyrosine kinase inhibitors are now being used for which leukemia?
CML
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Where doe lymphocytes accumulate in CLL?
bone marrow
lymph tissue
spleen
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What are the s/s of chronic lymphocytic leukemia? What do you find on PE?
asymptomatic
hepatosplenomegaly
lymphadenopathy
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A majority of cases of CLL are diagnosed after which age?
50
264
What is hyperleukocytosis?
hyperviscosity
WBC greater than 150
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What is the risk with hyperleukocytosis?
ischemia and infarct
266
Tumor lysis syndrome can lead to?
renal failure
267
What is the goal of pallatative care?
improve quality of life for both the patient and the family
provide relief from the sx and stress of illness
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What surgery will you do to cure the cancer?
remove the entire tumor
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What surgery will you do to allow for adjuvant therapy?
debulking
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What surgery will you do for palliation?
pain relief and decrompression
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What is done to confirm metastasis and for removal of regional metastases?
lymph node biopsy
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Lymph node biopsy is done to..
predict prognosis
plan adjuvant therapy
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What does a negative sentinal node biospy tell you?
suggests that cancer has not yet spread to nearby lymph nodes or organs
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What does a positive SLNB tell you?
cancer is present in the sentinel lymph node and that it may have spread
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What are the two main cancers setinal node biopsy is used for?
breast and melanoma
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What is the most common form of radiation?
external beam radiation
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What is external beam radiation?
pointing an external beam of ionizing radition precisely at the tumor site
278
What is internal beam radiation?
placing seeds, ribbons or capsules that contain a radiation source into the body or near the tumor at time of surgery of biopsy
279
What can chemo be used for?
shrink tumor (neoadjuvant)
destroy remaining cancer cells after surgery or radiation (adjuvant)
make other therapies more effective
destroy cancer cells that return or spread
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What is hormal therapy mostly used for?
breast and prostate cancers
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What is the most commen hormonal therapy?
tamoxifen
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Hormone therapy works by..
adding, blocking or removing hormones from the body to slow or stop the growth of cancer cells
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Drugs that take the brakes off the immune system which helps to recognize and attack cancer cells
checkpoint inhibitors
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immunotherapy that take T cells from the patients bood, mixes them with a special virus that makes the T cells learn how to attach to tumor cells then gives the cells back to the patient so they can kill the cacner is..
CAR T cell therapy
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immunotherapy that uses cytokines to simulate the immune cells to attack cancer is?
cytokines
286
Who should not do myeloablative prep before stem cell transplant?
heavilty treated patients
older/compromised
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What non malignant diseases can you use stem cell transplants for?
MS
immue deficiencies
sickle cell anemia/thalassemia
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From the the patients own stem cells
autologous
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stem cells from another person
allogeneic
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