A4M CORE REVIEWS ANSWERS AND QUESTIONS SET
A+
✔✔menopause affect on thyroid hormone - ✔✔Common for thyroid problems to appear
at menopause because your ovaries have thyroid receptors and your thyroid gland has
ovarian receptors. Loss of E2 and testosterone from your ovaries that occurs at
menopause can have an effect on your thyroid.
✔✔top 5 cardiovascular risk factors - ✔✔HTN
DM
dyslipidemia
obesity
smoking
✔✔how to test for more in depth understanding of top 5 <3 risk factors? - ✔✔24 hour
ambulatory BP monitoring
advanced lipid profiles
dysglycemic parameters
visceral obesity with effects of adipokines
inflammation
oxidative stress
immune vascular dysfunction
✔✔three finite vascular endothelial responses - ✔✔inflammation
oxidative stress
vascular immune dysfunction
✔✔how many risk factors for CHD? - ✔✔400
✔✔examples of cell membrane insult - ✔✔high BP
LDL cholesterol
glucose
microbes
toxins
heavy metals
,homocysteine
✔✔BP risk for CVD starts at what BP? - ✔✔110/70
✔✔risk for LDL cholesterol and fasting glucose causing reduction in NO in the
endothelium starts at what level? - ✔✔cholesterol 60 mg/dL
glucose 75 mg/dL
✔✔what oxidizes and modifies LDL cholesterol inside the vessel wall? - ✔✔free radicals
and glycation
✔✔how are foam cells formed? - ✔✔modified LDL is consumed by scavenger receptors
(SR-A and CD-36) on macrophages
✔✔balance of vascular disease - ✔✔vascular injury- angiotensin II and endothelin
vascular repair- endothelial progenitor cells (produced in bone marrow)
✔✔oxidative stress - ✔✔reactive oxygen species
reactive nitrogen species
both are increased in the arteries and kidneys and with a decreased oxidative defense
an imbalance between ROS and RNS and the anti-oxidant defense mechanisms
✔✔inflammation - ✔✔increased in the vasculature and kidneys
increased CRP, leukocytosis, neutrophils
decreased lymphocytes
increased RAAS in the kidney
✔✔autoimmune dysfunction - ✔✔of the arteries and kidneys
increased WBC and involvement of CD4 T helper cels and CD8 cytotoxic cells
cytokine production, central nervous system stimulation and renal damage
stimulation of ATR1, PPAR, TLR and direct stimulation of T cells on the endothelium
and vascular smooth muscle
release pro inflammatory mediators- IL, TNF alpha, IFN- gamma
✔✔biomechanical infinite insults - ✔✔BP
pulse pressure
shear stress
oscillatory pressure within the arterial system
✔✔where do most plaques form? - ✔✔bifurcation of arteries
,✔✔biochemical infinite insults - ✔✔nutritional factors
microbes
sterile antigens
environmental toxins
✔✔endothelial cell receptors that mediate interaction between insults and downstream
mediators - ✔✔pattern recognition receptors
toll like receptors
nod like receptors
caveolae
✔✔cardiovascular post prandial phenomena - ✔✔atherosclerosis, endothelial
dysfunction, and vascular disease are caused by ingestion of sodium, refined carbs, sat
fats/trans fats
trigger glucotoxicity, triglyceride toxicity, vascular endotoxemia, inflammation, oxidative
stress, immune dysfunction
✔✔how to help prevent post-prandial endothelial dysfunction? - ✔✔eating low GI foods
mono and poly unsaturated fats
polyphenols
antioxidants
✔✔how many years is vascular disease sub clinical prior to a cardio event? - ✔✔10 to
30 years or more
✔✔earliest functional abnormality in the vascular system - ✔✔endothelial dysfunction
then arterial compliance changes, stiffness, and elasticity
✔✔excessive BP dipping associated with? - ✔✔increased risk of ischemic stroke
✔✔reverse BP dipping is associated with? - ✔✔increased risk of intracerebral
hemorrhage
✔✔BP increase of _/_ doubles cardiovascular risk - ✔✔20/10
✔✔before age 50, _ BP predicts risk best? - ✔✔diastolic
✔✔after age 50, _ BP predicts risk best? - ✔✔systolic
✔✔primary driving cardiovascular risk related to LDL cholesterol? - ✔✔number of LDL
particle number (LDL-P and apolipoprotein B particles)
, ✔✔most protective cardiovascular risk factor related to lipids? - ✔✔HDL-P with larger
HDL type 2b being second
✔✔dysfunctional HDL - ✔✔more than 85 mg/dL
✔✔very atherogenic and thrombogenic - ✔✔VLDL
triglycerides
remnant particles
✔✔larger number and size of HDL are more efficient at what? - ✔✔reverse cholesterol
transport
✔✔FBS over 75 mg increased CHD by what percent per increase of 1 mg/dl? - ✔✔1%
induces endothelial dysfunction
✔✔FBS of 100 mg increases risk of CHD by? - ✔✔25%
✔✔2 hour GTT over 110 mg increases CHD by how much per 2 mg/dL? - ✔✔2%
✔✔2 hour GTT result of 140 mg increases risk of CHD and MI by? - ✔✔60%
✔✔what does insulin resistance do? - ✔✔creates inflammation
reduces NO levels
causes endothelial dysfunction and vascular disease
through the mitogenic activated protein kinase (MAPK) pathway which is atherogenic
and induces hypertension as opposed to the phophatidylinositol 3 kinase (PI3K)
pathway
✔✔specific tests to identify inflammation - ✔✔HS-CRP
✔✔specific tests to identify oxidative stress: - ✔✔oxLDL and myeloperoxidase
✔✔how to increase NO and eNOS? - ✔✔oral nitrates/nitrites, beet root juice/extracts,
dark
green leafy vegetables, cruciferous vegetables, polyphenols, vitamin C,
arginine, methylarginines, citrullene, grapefruit juice with PDE inhibitors,
PDE inhibitors ( viagra, cialis, levitra ), BH4, folate, B vitamins, NADH,
NADPH, glutathione(GSH), whey protein, selenium, sulfhydryls, thiols ( Rlipoic
acid, NAC, MSM), curcumin, quercetin.
✔✔ADMA and DDAH relation to NO - ✔✔ADMA, an endogenous L-arginine analogue,
reduces NO production by inhibiting the activity of NOS. ADMA levels in turn, are
A+
✔✔menopause affect on thyroid hormone - ✔✔Common for thyroid problems to appear
at menopause because your ovaries have thyroid receptors and your thyroid gland has
ovarian receptors. Loss of E2 and testosterone from your ovaries that occurs at
menopause can have an effect on your thyroid.
✔✔top 5 cardiovascular risk factors - ✔✔HTN
DM
dyslipidemia
obesity
smoking
✔✔how to test for more in depth understanding of top 5 <3 risk factors? - ✔✔24 hour
ambulatory BP monitoring
advanced lipid profiles
dysglycemic parameters
visceral obesity with effects of adipokines
inflammation
oxidative stress
immune vascular dysfunction
✔✔three finite vascular endothelial responses - ✔✔inflammation
oxidative stress
vascular immune dysfunction
✔✔how many risk factors for CHD? - ✔✔400
✔✔examples of cell membrane insult - ✔✔high BP
LDL cholesterol
glucose
microbes
toxins
heavy metals
,homocysteine
✔✔BP risk for CVD starts at what BP? - ✔✔110/70
✔✔risk for LDL cholesterol and fasting glucose causing reduction in NO in the
endothelium starts at what level? - ✔✔cholesterol 60 mg/dL
glucose 75 mg/dL
✔✔what oxidizes and modifies LDL cholesterol inside the vessel wall? - ✔✔free radicals
and glycation
✔✔how are foam cells formed? - ✔✔modified LDL is consumed by scavenger receptors
(SR-A and CD-36) on macrophages
✔✔balance of vascular disease - ✔✔vascular injury- angiotensin II and endothelin
vascular repair- endothelial progenitor cells (produced in bone marrow)
✔✔oxidative stress - ✔✔reactive oxygen species
reactive nitrogen species
both are increased in the arteries and kidneys and with a decreased oxidative defense
an imbalance between ROS and RNS and the anti-oxidant defense mechanisms
✔✔inflammation - ✔✔increased in the vasculature and kidneys
increased CRP, leukocytosis, neutrophils
decreased lymphocytes
increased RAAS in the kidney
✔✔autoimmune dysfunction - ✔✔of the arteries and kidneys
increased WBC and involvement of CD4 T helper cels and CD8 cytotoxic cells
cytokine production, central nervous system stimulation and renal damage
stimulation of ATR1, PPAR, TLR and direct stimulation of T cells on the endothelium
and vascular smooth muscle
release pro inflammatory mediators- IL, TNF alpha, IFN- gamma
✔✔biomechanical infinite insults - ✔✔BP
pulse pressure
shear stress
oscillatory pressure within the arterial system
✔✔where do most plaques form? - ✔✔bifurcation of arteries
,✔✔biochemical infinite insults - ✔✔nutritional factors
microbes
sterile antigens
environmental toxins
✔✔endothelial cell receptors that mediate interaction between insults and downstream
mediators - ✔✔pattern recognition receptors
toll like receptors
nod like receptors
caveolae
✔✔cardiovascular post prandial phenomena - ✔✔atherosclerosis, endothelial
dysfunction, and vascular disease are caused by ingestion of sodium, refined carbs, sat
fats/trans fats
trigger glucotoxicity, triglyceride toxicity, vascular endotoxemia, inflammation, oxidative
stress, immune dysfunction
✔✔how to help prevent post-prandial endothelial dysfunction? - ✔✔eating low GI foods
mono and poly unsaturated fats
polyphenols
antioxidants
✔✔how many years is vascular disease sub clinical prior to a cardio event? - ✔✔10 to
30 years or more
✔✔earliest functional abnormality in the vascular system - ✔✔endothelial dysfunction
then arterial compliance changes, stiffness, and elasticity
✔✔excessive BP dipping associated with? - ✔✔increased risk of ischemic stroke
✔✔reverse BP dipping is associated with? - ✔✔increased risk of intracerebral
hemorrhage
✔✔BP increase of _/_ doubles cardiovascular risk - ✔✔20/10
✔✔before age 50, _ BP predicts risk best? - ✔✔diastolic
✔✔after age 50, _ BP predicts risk best? - ✔✔systolic
✔✔primary driving cardiovascular risk related to LDL cholesterol? - ✔✔number of LDL
particle number (LDL-P and apolipoprotein B particles)
, ✔✔most protective cardiovascular risk factor related to lipids? - ✔✔HDL-P with larger
HDL type 2b being second
✔✔dysfunctional HDL - ✔✔more than 85 mg/dL
✔✔very atherogenic and thrombogenic - ✔✔VLDL
triglycerides
remnant particles
✔✔larger number and size of HDL are more efficient at what? - ✔✔reverse cholesterol
transport
✔✔FBS over 75 mg increased CHD by what percent per increase of 1 mg/dl? - ✔✔1%
induces endothelial dysfunction
✔✔FBS of 100 mg increases risk of CHD by? - ✔✔25%
✔✔2 hour GTT over 110 mg increases CHD by how much per 2 mg/dL? - ✔✔2%
✔✔2 hour GTT result of 140 mg increases risk of CHD and MI by? - ✔✔60%
✔✔what does insulin resistance do? - ✔✔creates inflammation
reduces NO levels
causes endothelial dysfunction and vascular disease
through the mitogenic activated protein kinase (MAPK) pathway which is atherogenic
and induces hypertension as opposed to the phophatidylinositol 3 kinase (PI3K)
pathway
✔✔specific tests to identify inflammation - ✔✔HS-CRP
✔✔specific tests to identify oxidative stress: - ✔✔oxLDL and myeloperoxidase
✔✔how to increase NO and eNOS? - ✔✔oral nitrates/nitrites, beet root juice/extracts,
dark
green leafy vegetables, cruciferous vegetables, polyphenols, vitamin C,
arginine, methylarginines, citrullene, grapefruit juice with PDE inhibitors,
PDE inhibitors ( viagra, cialis, levitra ), BH4, folate, B vitamins, NADH,
NADPH, glutathione(GSH), whey protein, selenium, sulfhydryls, thiols ( Rlipoic
acid, NAC, MSM), curcumin, quercetin.
✔✔ADMA and DDAH relation to NO - ✔✔ADMA, an endogenous L-arginine analogue,
reduces NO production by inhibiting the activity of NOS. ADMA levels in turn, are
