Exam 3: Cancer, Hem, Vasc, Card Flashcards
cancer, hemo, vasc, cardiac
tumor
localized swelling
neoplasm
tumor caused by hyperplasia
hyperplasia
cell proliferation
benign neoplasm
noninvasive, encapsulated neoplasm that resembles tissue of origin
malignant neoplasm
cancer
divided rapidly and unremittingly
characteristics of a malignant neoplasm
anaplasia
invasive
poorly differentiated
anaplasia
undifferentiated
not normal adult cells
cancer grading
based on histology
1. well differentiated/mild dysplasia
2. moderate differentiated/moderate dysplasia
3. poor differentiated/severe dysplasia
4. moderate anaplasia
5. severe anaplasia
cancer staging
based on spread
0- in situ
1- localized
2- limited spread within an organ
3. regional spread and to lymph nodes
4- distant metastasis
cellular characteristics of malignancy
autonomous
anaplastic
dysplastic
immortal
angiogenic
autonomous
self sufficiency to growth signals (being independent of normal cellular control)
insensitivity to antigrowth or apoptotic signals
anaplastic
loss of differentiation
dysplastic
loss of contact inhibition/anchorage dependence
immortal
cells do not reach the Hayflick limit of cell division
cells resist apoptosis
angiogenic
cells receive own blood supply (VEGF)
carcinoma
cancerous tumor of epithelial origin
sarcoma
cancerous tumor of mesenchymal origin
mole
benign neoplasia of melanocyte
melanoma
malignant neoplasia of melanocyte
fibroma
benign proliferation of fibroblasts
fibrosarcoma
malignant neoplasia of fibroblasts
osteoma
benign neoplasia of osteocytes
osteosarcoma
malignant neoplasia of osteocytes
teratoma
monster cancer
malignant only
leukemia
malignant neoplasia of bone marrow
malignant only
signs of melanoma
asymmetric
borders uneven
coloring uneven
diameter changing
enlarging
post oncogens
cell cycle activators
gain of function
tumor suppressor genes
cell cycle inhibitors
loss of function
multi hit theory
multiple mutations are needed before malignancy occurs
based off of idea that incidence vs age is nonlinear
carcinogens
base analogs
radiation
chemical mutagens
intercalators
viruses
intercalators
things that fit between the 2 strands of DNA helix
chemotherapy drug goal
stop cell replication and division
radiation goal
damage to DNA to shrink tumor
a blood tube looks like…
erythrocytes on bottom
leukocytes + platelets middle
plasma stays on top
plasma
55% of total blood
91% water, 7% protein, 2% other organic molecules and electrolytes
protein
albumin- maintains osmotic pressure
globulins
fibrinogen
organic molecules
glucose
amino acids
globulins
alpha- HDL, steroids
beta- LDL, transferrin
gamma- antibodies, IgG
formed elements
45% of total blood
erythrocytes
platelets
leukocytes
what produces platelets
megakaryocytes
leukocytes
neutrophils 60%
lymphocytes 30%
monocytes,eosinophils,basophils 10%
lymphocytes
T cells 70%
B cells 25%
NK cells 5%
erythrocytes and platelets…
do NOT have nuclei
are NOT true cells
no nuclei=
no DNA
unable to transcribe RNA
therefore no protein
have a short life span because they cannot repair damage
where are formed elements produced
hematopoietic stem cells
aka pluripotent cells
located in the bone marrow
what gives erythrocytes their red color
hemoglobin
300Hgb per RBC
shape of erythrocyte
biconcave disc
oxyhemoglobin
more red
oxygen bound
deoxyhemoglobin
changes shape and color
is blue/purple
nonoxygenated
oxygen hemoglobin dissociation curve
O2 binds Hgb in a cooperative way
nonlinear, sigmoidal
“to the right”
binding oxygen more loosely
Hgb dumps off O2 more efficiently
factors that shift curve to the right
increased H ions, decreased pH
increased PCO2, decreased pH
increased temp
increased DPG (r/t high altitude or congenital heart disease)
spleen
lymphoid organ
houses leukocytes
acts as a blood filter
hematopoiesis
occurs in axial skeleton bone marrow
blood formation
adults have
2 alpha and 2 beta
fetuses have
alpha, beta, gamma
higher affinity for Hgb
erythropoietin
hormone epo
stimulates bone marrow to produce RBCs
erythropoesis
formation of red blood cells
anemia
erythrocyte deficit
deficiency of vitamin b12 or folic acid
vitamin b12 and folic acid are
necessary but not sufficient
stem cell considerations
can make more stem cells
can differentiate
erythropoietin feedback
1.hypoxia
2. renal cortex senses hypoxia
3. erythropoietin secreted
4. bone marrow stimulation
5. bone marrow stimulation triggers erythropoiesis
6. normoxia
7. renal cortex senses normoxia
8. decreased erythropoietin
anytime the kidneys sense hypoxia
epo is produced until tissue reaches normal oxygen level
4 heme’s
heme oxygenase
biliverdin
biliverdin reductase
bilirubin
jaundice
accumulation of bilirubin r/t too erythrocyte degradation
etiology of anemia
hemorrhage
decreased erythropoiesis
increased erythrocytic destruction
koilynchia
spoon nails r/t anemia
glossitis
tongue inflammation
loss of papillae
r/t anemia
clinical manifestations of anemia
claudication
dyspnea
dizziness
pallor
compensatory mechanisms of anemia
tachycardia
tachypnea
increased DPG in blood
increased renin+ erythropoietin
hemolytic anemia
normocytic and normochromic
maturing normally but making less RBC’s
iron deficiency anemia
microcytic and hypochromic
small cells with less Hgb pigment
pernicious anemia
macrocytic and normochromic
large unmature cells r/t vitb12 deficiency
sickle cell anemia
congenital
stack and clog arteries
polycthemia
erythrocyte surplus
sed rate
erythrocyte sedimentation rate
high sed rate
sink faster
inflammation, diabetes, old age, cancer, anemia
low sed rate
sink slower
sickle cell, young age, polycythemia
hemostasis
blood clotting
damaged endothelial lining triggers thrombocytes, VWF, fibroblasts
therefore fibrinogen then fibrin
how does fibrinogen form fibrin
fibrinogen must be cut off to activate and form fibrin
how is clot formed
thrombocytes grab fibrin
left side of heart
sends oxygenated blood to body tissues through aorta
right side of heart
sends deoxygenated blood to the lungs
arteries
take blood away from heart
increased pressure decreased volume
no valves
thick walls (especially tuna media)
veins
take blood into the heart
decreased pressure
increased volume
valves
thin walls
what cells are in tunica intima
endothelial cells
what cells are in tunica media
pseudostratified cells
what cells are in tunica adventitia
fibroblasts
vasoconstriction causes
increased blood pressure
vasodilation causes
decreased blood pressure
blood vessel resistance increases with
increased blood viscosity
increase length of vessel
primary hypertension
idiopathic or genetic
manifestations: nose bleeds, headache
if a protein ends in -ogen
it needs to be cleaved to become activated
thrombus
stationary clot
embolus
travelling clot
Right sided embolus
pulmonary embolism
left sided embolus
MI or stroke
turbulent blood flow causes
clotting
renin-angiotensin aldosterone system
- angiotensinogen (inactive protein)
- renin cleaves off part of angiotensinogen, becoming angiotensin
- angiotensin is modified by ACE enzyme to form angiotensin 2
- angiotensin 2 tells kidneys to retain fluid and vessels to constrict
- constricted vessels=increased blood pressure
what does renin do
cleaves off a part of angiotensinogen to become angiotensin
what does ACE enzyme do
modifies angiotensin to form angiotensin 2
what does angiotensin 2 do
tells kidneys to retain fluid and vessels to constrict
what does constricted vessels do
increases blood pressure
atherosclerosis
arterial hardening caused by waxy deposits in the wall of the artery
causes turbulent blood flow
aneurysm
localized dilation of vessel wall
only surgical treatment
false aneurysm
clot forms from hemorrhage related to damage of adventitia
most common site of aneurysm
descending aorta
bc less supporting structures
aortic dissection
a tear through the tunica intima and media of the aorta.
often r/t trauma
thromboangiitis obliterans
occlusion of artery
manifestations: claudication, artery obstruction
treat w vasodilators
high risk: nicotine + testosterone
varicose veins
pooled blood leading to bulging veins
valve damage and decreased connective tissue support
deep vein thrombosis
blood clot forms in a large vein
superior vena cava syndrome
progressive occlusion of super vena cava
causes distention of upper vasculature (upper body, facial edema)
MRA vs CAT scan
MRI has higher resolution
apex of heart
bottom of the heart (ventricles)
points posterior
intraventricular septum
between left and right ventricles
atria
thin walled because have less pressure
semilunar valves
aortic and pulmonic
aortic valve
between left ventricle and aorta
pulmonic valve
between right ventricle and pulmonic artery
atrioventricular valves
tricuspid and mitral valve
tricuspid valve
right AV valve
btw right atria and ventricle
mitral valve
left AV valve, “bicuspid”
between left atria and ventricle
chordae tendonae
hold valves in place and prevent regurgitation
cardiac cycle
- atrial systole
- ventricular contraction
- ejection
- ventricular relaxation
- ventricular filling
atrial systole
blood pushed into ventricles
ventricular systole
isovolumetric contraction so pressure in ventricles equals pressure in arteries
ejection
ventricular pressure increases and exceeds pressure in arteries
ventricular diastole
pressure drops so ventricles relax
ventricular filling
blood from veins enter the heart as vein pressure exceeds ventricular pressure
endocardium
innermost layer with endothelial cells
myocardium
muscle middle layer with striated skeletal cells
epicardium
“serious pericardium”
“visceral” inner layer of pericardiam
parietal pericardium
outermost layer
cardiac tamponade
excess fluid in pericardial space, making the heart fluid deficient
atrial systole
AV valves open and SV valves close
ventricular systole
AV valves close and SV vaves open
2 major arteries
Left coronary artery
Right coronary artery
“widow maker”
LAD (anterior interventricular)
coronary angiogram
great for viewing coronary arteries
utilizes contrast dye and CXR
cardiomyocytes
heart muscle cells
striated w myosin + actin
intercalated discs
contain proteins that connect one cardiomyocyte to another.
contain gap junctions
gap junctions
allows for electric conduction
when one contracts, the other contracts= functional snysynium
functional synsynium
when one contracts the other contracts
depolarize
contract
repolarize
relax
P wave
atrial depolarization
QRS complex
ventricular depolarization
T wave
ventricular repolarization
PR interval
measure of time interval from atrial electrical activity to ventricular electrical activity
Na/K pump
3 Na out
2 K in
during depolarization…
Na channels open and flood in, opening Ca channels which flood Ca in, making the myocardial cells squeeze
1st heart sound
closure of AV valves
QRS complex
ventricular depolarization
pressure increases
2nd heart sound
closure of SL valves
T wave
ventricular repolarization
decreased pressure
premature ventricular contraction (PVC’s)
spontaneous depolarization of ventricular cardiomyocytes
feels like heart is skipping a beat
can be treated by cardiac ablation
heart block
miscommunication btw atria and ventricles
due to damage to the heart’s conduction system
coronary artery disease (CAD)
atherosclerosis in coronary artery
leads to MI bc thrombus that forms and causes ischemia
anginapectoris
chest pain due to intermittent myocardial ischemia
treat w aspirin + nitro
angioplasty
inflate a catheter balloon to compress plaque
stent placement
inflate a catheter balloon containing a metal stent to hold artery open more permanently
acute coronary syndrome
MI, complete occlusion
irreversible damage
troponin I and II present
fluroscopy
real time xrays used for coronary angiogram
inflammation always =
fibrotic deposition
coronary artery bypass graft (CABG)
use a vein from the leg to bypass an occlussion in the heart
stenosis
stiffening
prevents total valvular opening and closing
stenosed mitral valve
allows regurgitation into left atrium and prevents blood flow into left ventricle
mitral valve prolapse
blood gets into left atrium rather than left ventricle out thru aorta and out to body
doppler echocardiogram
ultrasound visualizing blood
confirms heart sounds
cardiomyopathy
heart muscle disease
3 types: dilated, hypertrophic, restrictive
subtle changes in heart proteins can cause
dilated cardiomyopathy
decreased ejection fraction
hypertrophic cardiomyopathy
heart becomes thick and distorted
often occurs as compensation
restrictive cardiomyopathy
stiffening of myocardium
doesnt allow heart to fill well
ductus arteriousus
shunts blood from pulmonary arteries to aorta
foramen ovale
shunts blood from right atria to left atria
2 mechanisms in congential hearts
ductus arteriosus and foramen ovale
arterial septal defect
hole between atria when foramen ovale does not collapse
ventricular septal defect
hole between ventricle
more serious