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60 Cards in this Set

  • Front
  • Back
What are the three non-modifiable risk factors for atherosclerosis?
Age
Sex
Dyslipoproteinemia
What are the five modifiable risk factors for atherosclerosis?
Dyslipidemia
Diabetes
Obesity
Smoking
Hypertension
Where are LDL receptors located
Hepatocytes
Adipocytes
Adrenal cells
How fast is LDL endocytosed?
3 minutes
What are the roles of Ox-LDL?
Cause endothelial cells to produce MCP-1 (monocyte transmigration)
Promote monocyte differentiation
Initiate M-CSF generation from endothelial cells (Express scavenger receptors on macrophage surface)
Phagocytosed by macrophage to form foam cells
What is released by macrophages and what do they do
TNF-alpha
IL-1
Induce endothelial cells to express VCAM-1, P-selectin
What is the optimal LDL
< 100 mg/dL or 2.59 mM
what is considered high LDL
> 160 mg/dL or 4.14 mM
Limb leads
Lead I, II, III, aVF, aVR, aVL
Chest leads
V1-6
Symptoms of cardiac arrythmias
Palpitations, dizziness, fatigue, loss of conciousness, shortness of breath, blood stasis
What phase of the miocardial action potential is affect by change in automaticity
Phase 4 slope increases and allows for threshold potential to be reached more rapidly
Common cause of increased automaticity arrythmia
ischemia results in anaerobic metabolism (decreased activity of Na/K ATPase)
three conditions that cause re-entry
pathways longer than normal (dilated heart)
perkinje fibre transmission is slow
decreased refractory period (often due to drugs)
How is atrial flutter distinguished from atrial fib. on an ECG
defined P wave
slower atrial beat
How long before V. fib. causes death
1-3 minutes
What is natriuretic factor
released by atrial/ventricular myocardium to inhibit Na reabsorption in distal tubules - diuresis
clinical hypertension
≥140/90 mm Hg in ≥2 doctor visits
What proportion of HTN patients are controlled?
16%
What is pheochromocytoma
excessive production of adrenaline
major risk factors for hypertension
obesity, smoking, hyperinsulinemia, high salt, high fat, stress, genetic factors
What are the components of bone
Bone cells
Type 1 collagen (Protein matrix)
Hydroxyapatite
Growth factors (TGFb, IGF-1)
Other matrix proteins (fibronectin, osteocalcin, osteopontin)
What are osteocytes?
Machanoreceptors/effectors emedded in bone
What increases RANKL/OPG ratio
PTH
Vitamin D
Some cytokines
What decreases RANKL/OPG ratio
Estrogen
TGF-b
Mechanical force
How does osteoclast initially dissolve minerals
H+ pumped out by H+ ATPase
How does osteoclast dissolve organic matrix
Cathepsin K
Molecular activators of bone remodeling
PTH, vitamin D, thyroid hormone, I/TNFa
Inhibitors of bone remodelling
Calcitonin
Estrogen
At what age does bone resorption=fromation
25-35
what happens to bone as you age
remodeling cycles increases in frequency
imbalance of osteoclast/blast activity
loss of estrogen in women with menopause
cortical bone thins and becomes porous
trabecular bone weakens due to decreased bone density, increase # and depth of resorption pits, loss of trabecular connectivity and perforation of trabecular plates
effect of estrogen
neg - osteoclast precursors
neg - osteoclast
pos. lifespan, anabolic activity
two functions of kidneys
rid of waste
volume and composition control
why do we care about sodium
predominant ion of ECF
movement of sodium controlled by transport mechanisms
what proportion of CO does kidneys filter
20%
how fast does kidney filter
180 L/day
what is moved in proximal tubule
nutrients
Na/K ATPase
Na/H exchanger
Carbonic anhydrase
Organic acid secretors
what crosses at the loop
descending thin is freely permeable to water
sodium, chloride, potassium reabsorption
what crosses at distal
Na/Cl transporter
Hydrogen
What crosses the collecting duct
water
Na channel - resorption preferred
K channel - secreted
Blood clot
platelet, trapped RBCs, fibrin
Virchow's Triad
Blood stasis
Hypercoagulability
Endothelial injury
Mortality rate due to heart failure
50% at 5 years
Role of inflammation in myocardial ischemia
release of TNF, IL-6 and IFN-gamma stimulate endotherlial cells and activate macrophages that fill with Ox-LDL
What is prinzmetal or variant angina
uncommon episodic angina that happens at rest due to coronary vasospasm
factors that determine infarct size
severity and duration of ischemia
size
collateral coronary circulation
spontaneous lysis of cornary thrombus
effects of therapy
two cardiac enzyme tests
troponins T and I (rise for 10 days)
creatine kinase (elevated for 72 hours)
how do you detect silent MI
exercise stress test
pericarditis
inflammation of pericaridum
fibirinous or fibrohemorrhagic
2-3 days post-MI
Chronic IHD with heart failure
progressive heart failure
enlarged heart secondary to left ventricular hypertrophy and dilation
gray-white scars of healed infartcs
sudden cardiac death
within 1 hour of symptoms (or without)
most common mechanism is lethal arrhythmia
erythropoiesis during second trimester
liver, spleen, lymph nodes
major type of fetal Hb
HbF
2 alpha, 2 gamma chains
decreased proliferation/differentiation of stem cells
aplastic anemia, renal failure, endocrine disorders
decreased maturation of erythroblasts
B12 deficiency, folic acid deficiency
decreased Hb synth
iron deficiency (decreased heme)
decreased globin synth (thalassemia)
folic acid/B12 deficiency
Macrocytic normochromic anemia
decrease in RBC, WBC, platelets
large hypersegmented neutrophils
bone marrow hypercellular
ineffective hematopoiesis and RBC destruction
Thalassemia
microcytic hypochromic anemia
erythroid hyperplasia in bone marrow
extramedullary hematopoiesis (liver, spleen)
increased iron absorption
increase in HbF/A2 to compensate
Iron deficiency
microcytic hypochromic anemia
decreased erythroid progenitors
mimics chronic disease anemia
aplastic anemia
bone marrow failure
decreased WBC, RBC, Platelets
suppression of myeloid stem cells
due to infections, chemicals, radiation, drugs
hypocellular bone marrow
reversible or irreversible