EXAM 3 Flashcards
fibromuscular dyplasia will appear how?
can occur anywhere, but tends to look like beads on a string - tends to occur in the kidney
wht is conn syndrome
when you have a tumor in the zona glomerulosa that releases excess aldosterone –> Na+ retention and SVR increase
explain DOC hypersecretion
increased ACTH from the anterior pituitary for any reason leads to hypersecretion of deoxycortisone, an aldoserone precurosor –> retention of Na+
explain GRA: Glucocortocoid remediable aldosteronism
genes encoding aldosterone synthase and 11b hydroxylase are linked during embryogenesis
- get hypersecretion of glucocortocoids and aldsterone
- have very severe HTN that starts early in life
how to treat GRA
glucocortocois
three adrenal gland disorders
Con syndrome, DOC hypersecretion, glucocortocoid remediable aldosteronism
cushing’s syndrome
incidence of HTN is greater in cushing’s - excess glucocortocoid. this increases angiotensinogen
most common risk of cushings
oral corticosteroids
symptoms of cushings
buffalo hump, broomstick arm+ legs,
pheochromacytoma
increased NE from the adrenal medulla leading to an increase in systolic and diastolic pressure
symptoms of pheo
palpittions, hypertension, glycosuria and extree systolic HTN
how do natriuretic hormones work
they dump Na+ into the urine, but cause Ca to accumulate –> vascular smooth muscle contraction
2x more likely to develop ____ than ____ in smoking
PAD
explain the ankle-brachial index
on the arms and ankles the BP should be the same, but in peripheral artery disease, sometimes it is not
in PAD, a drop of ____ as you go down the leg is significant
20mmHg
how do you treat PAD
- smoking cessation, HTN control, statin,
- antiplatelet therapy: ASA
- exercise
the timing of surgical repair of an aortic aneurysm is related to
the diameter and the rate of increase
pulsatile abdominal mass is a
abdominal aortic aneurysm
what will you find in a thoracic abdominal aneurysm
cystic medial necrosis - a mucoid material accumulation in the media of the aorta
risk factors of AAA
smoking, male, atherosclerosis
descending thoracic AA due to
atherosclerosis
ascending thoracic AA due to
bicuspid aortic valve, connective tissue disease, syphillis
genetic factors leading to an ascending thoracic AA
Marfan, ehlers danlos and loeys deitz
defect in marfan
FBN1
defect in ehlers danlos
type III collagen
defect in loeys deitz
TGFBR
ideal size to operate on an aortic aneurysm
5cm
what is the genetic inheritance pattern of marfan
autosomal dominant
what tears in an aortic dissection
intimina
where is the blood located in an aortic dissection
in the media
what structures can a debakey typeI/ ascending Aortic dissection damage
the aortic annulus and RCA
abrupt onset of severe chest pain radiating to the back
aortic dissection
what does a negative D-dimer test tell you about aortic dissection
rules out dissection
how does one treat an aortic dissetion
1) lower BP + HR with IV labetolol and nitroprusside, BB if the BP is already low to decrease HR
what do we want to AVOID in aotic dissections
pure venous dillators such a nitroglycerin
treating type A dissection
surgical emergency
mutation leading to vascular ehlers danlos
COL3A
best way to diagnose aortic dissecction
Computer thomography angiography
how to diagnose PAD
non-invasive flow studies
type of arteriolar disease seen in diabetes
hyaline arteriosclerosis
what cases the hyerplastic appearance of arteriosclerosis
smooth muscle proliferation
acute renal failure from which type of arteriosclerosis
hyperplastic
lipo proteins that are pro-atherogenic
cylomicrons/ VLDL
LDL - apo B (90% of apo B is LDL)
anti atherogenic lipoproteins
HDL
Apo A
what parameter of HDL so i care about
how many of the particles you have, not how much cholesterol is in the body
higher LDL leads to an increased risk of
coronary artery disease
what does HDL take from the VLDL and LDL
cholesterol
and takes it from the periphery and back to the liver.
most genetic causes of dyslipidemia are due to a
LDL receptor defect
if LDL> ______ you are likely to have a heterozygrous LDL R problem
LDL>190
when Triglycerides are mre than 1000 you suspect ____ and worry about what condition
genetic defect and pancreatitis
drugs that can make your cholesterol very high
protease inhibitors for HIV
corticosteroids and immunosupressant like rapamycin
major statins
atrovastatin and rosuvastatin
what do statins do
they block the production of cholesterol by the liver
statin side effects
transaminitis - increase in ASL and ALT,
Rhabdomyalasis
rhabdomyalasis high risk population
advaced age, women, frailty, alcohol abuse
statin drug interaction that can put at risk for rhabdomyalysis
fibrates
what does ezetamide fo
blocks uptake fo bile acids back into the circulation
PCSK9 acts how
is a cofactor for the LDL receptor, which marks it for degredation. so the more PCSK9 you have the less LDL receptor and higher cholesterol
how do PCSK9 inhibitors work
if not PCSK9, LDL receptors stay on the liver all the time and are never broken down, so very low cholesterol in the circulation
golden standard for cholesterol treatments?
statins - most effective for reducing cardiovascular risk - and ezetamide
dyslipidemia is driven by _____ containing proteins
apo b on LDL and VLDL
what do fibrates decrease the most?
TAGs
what causes hyaline arteriolosclerosis
diabetes and HTN
most predicitive inflammatory marker of MI risk
CRP + Total cholesterol:HDL - markers of the acute phase repsonse
prostacyclin is a
vasodillator
Platelet aggrivating factor is a
vasoconstrictor
what do statins do to eNOS and what does eNOS do
statins inrease
where are nicotinic Ach receptors found
preganglionic synapse of PNS, SNS and at skeletal muscle post ganlgionic
post mi, cardiac arrhthmias occur
within 1st few days after Mi
post MI, fibrinous pericarditis occurs
1-3 days after MI
post Mi, papillary muscle rupture occurs
2-7 days
IC setpum rupture after an MI will occur
3-5 post Mi
aneurysm formation after an Mi will occur
5-14 days post MI
dressler syndrome occurs how long after an Mi
weeks-months
probability of death from CVD
47%
normal response of a vessel to acetycholine is to
dillate
what drugs promote eNOS function
statins
EXCESS NO CAN predispose to
shock
too little NO leads to
atherosclerosis
what molecue to chemokines use to attract an activate monocytes
monocyte chemoattractant protein-1 MCP-1
smooth muscle cels in atheroscelerosis secrete
collagen and elastin
what moleculae to platelets make that results in vasconstriction and anginal pain
TXA2
what is the singel most important determinany of stenosis for any given level of flow
the minimum cross sectional area within the stenosis
low ATP, due to MI, and inability to relax the LV leads to
diastolic dysfuntion
transient sarcomeric dyskinesis due to low O2 leads to
systolic sydfunction
what releases TPA
endothelial cells
what activates tpa
thrombin
what does tpa do
it converts plasmin to plasminogen, which breaks down fibrin
what is an inhibitor of thombolysis
plaminogen activator inhibitor, PAI-1
elevation in cardiac biomarkers in untable angina?
no
describe prinzmetal agina
episodic chest pain that occurs at rest, that is secondary to vasospasm
does prinzmetal angina respond to vasodillators?
yes, responds promtly to nitroglycerin
ST segment requirements for dianogsis of a STEMi
- St elevation in 2 contiguous leads or new LBBB
- St elevation = 1mm limb, and 2mm in precordial
which leads indicate an ateroseptal infarct
V1-V4
what artery would be occluded in an ateroseptal infarct
LAD
what leads indicate a lateral infarct
I, AVL, V5 and V6
what arteries supply the lateral heart
L circumflex and the LAD diagonal
what leads indicate an inferior infarct
II, III and Avf
what arteries supply the inferior part of the heart
RCA if right dominant
Lcx if left cominant
and mid LAd
see yellowing alone, how old is the Mi?
1-3 days
see yellow with rd borders, how old si the Mi
2-4 day range
no red or yellow, jsut mushy or necrotic, how old is the infarct
7-10 days old
red-grey infarct with red rim is how old?
more than 10 days
previous myocarditis pointsyou towards a diagnosis of
dilated cardiomyopathy
an s3 sound makes you think that the heart is
dilated
s4 heart sound makes you think the heart is
hypertrophic
hypertrophic cardioyopathy due to what mutation
b-myosin heavy chain
what disease is caused by defects in adhesion proteins such a desmosomes
arrhythmogenic right ventricular cardiomyopathy
describe arrhythmogenic right ventricular cardiomyopathy
the RV wall is thinned with fatty ifnilatrates and fobrosis
most common reason for a restrictive cardiomyopathy
amyloidosis
what is seen on histo in restricitive cardiomyopathies
eosinophilic protein deposited btw cardiac myositis
key sign in sarcoid cardiomyopathy
non caseating granulomas leading to a thick and stiffened paricardium
how to diagnose sarcoid cardiomyopathy
MRI
viral infections leading to myocarditis
group b coxackie and chagas disease
fibrinous/serofibrinous pricarditis is usally associated with what findings or conditions
pericardial rub and dresslers syndrome
myofilbrillar disarray seen in
hypertrophic idiopathic subaortic stenosis
organiss that infect vascular endothelial cells
Rickettsia, Orientsia
organisms that infect circulating granuocytes
Ehrlichia, Anaplasma
intrcellular pathogen that ifnects erythrocytes
Bartonella bacilliformis
most bacterial spread is via
lymphatic capillaries through the lymph nodes into the thoracic duct.
Prototype parasitic bloodstream pathology
malaria `
homes of a malria virus
in the misuito, in the RBC and in the liver hepatocyte
requirement to be on the blod borne pathoge list
characterized by a phase in which the microbes causing the disease may circulate in the blood for a prolonged period. They are therefore capable of being transmitted through blood or other potentially infectious materials.
histo findings in rheumatic fever
ashoff bodies and antischow cells
syptoms of aortic stenosis
Syndope
Angina
Dyspnea
pulsus parvus et tardus
pulsus parvus et tardus means
weak pulses w a delayed
murmur of aortic stenosis
crescendo-decrescndo murur radiating to the corotids
a late aortic stenosis murmur means
more severe
drugs to avoid in aortic stenosis
preload reducers such a diuretics and nitroglycerin
most coomon cause of aortic regurg
aortic root dilation
a wide pulse pressure points you towards which valve deformity
aortic insufficiency
in aortic regurg you want to to treat by
lowering the afterload
describe sound of aortic insufficiency
high pitched diasotlic
widely split S2 think
pulmonic stenosis
notched alongated sick looking p wave think
mitral stenosis
opening snap wiht loud first heart sound heard in
mitral stenosis
does a short or longer time between S2 and the opening snap worse?
shorter time btw OS and S2 is worse
main reason for mitral insufficiency
myxamatous degenertion
for mitral stenosis, what mediation should you NOT use
b blockers or negative inotropes
kleinfelters assocaited with
mitral valve prolapse
opening click heard btw S1 and S1 think
mitral valve prolapse
