cardio 1 Flashcards
causes of viral myocarditis
parvovirus B19, HHV-6, HIV, and adenovirus.
picorna (coxsackie)
signs of MI but no cardio markers elevated
unstable angina
which beta blockers from the selective type has an effect on B2 rec too
labetolol
pulsus parodoxus
seen in cardiac tamponade or constrictive pericarditis
decrease in pressure on deep insp
pulsus parvus et tardus
aortic stenosis
he patient’s history of pharyngitis 2 weeks ago and the palpable non-blanching skin lesions with arthritis and abdominal pain are classic signs of
HSP
small cell vasculitis
blood brain barrier composed of
Composed of three layers: pedicles (foot processes of astrocytes), a basal membrane, and capillary endothelial cells bound by tight junctions.
damage to tight junctions can lead to edema
what is the function of PDGF in atherosclerosis
binds to tyrosine kinase receptors and stimulates the transition of cells from the G1 phase to the S phase. PDGF is released at atherosclerotic lesion sites by platelets and macrophages and stimulates proliferation and migration of smooth muscles cells in the tunica intima,
how is the thrombus formed after atheroma
matrix metalloproteinases is thought to be responsible for breaking down the fibrous cap of an atheroma. Matrix metalloproteinases, which are secreted by inflammatory cells in the atheroma (e.g., macrophages), weaken the fibrous cap by breaking down the extracellular matrix. Subsequently, minor stress can rupture the fibrous cap and expose the atheroma’s highly thrombogenic lipid core. It is this event that then causes the acute, total obstruction of the vessel and subsequent myocardial infarction.
bronchial artery originates
from internal thoracic arteries
branch of thoracic aorta
LEFT originates directly from thoracic aorta
what happens in ischemic muscle
dysfunction of sarcoplasmic ca channel
production of lactid acid due to anaerobic resp
inc in H+…. this gets throw out and Na+ is absp in
Na brings water along —– cell swelling
idarucizumab
dabigatran reversal
direct thrombin inhibitor
used fro —- venous thromboembolism and a fib
drug prescribed in anaphylactic shock
how does it affect the pacemaker action potential
catecholamines
increase Na and ca influx in PHASE 4
adenosine also works on PHASE 4 —- increases the K conductance —– decreases HR
what phase determines Heart rate
PHASE 4
Nonbacterial verrucous thrombi on the undersurface of the mitral valve are suggestive of
licman sack
SLE
subacute endocarditis
strept viridians
opt res, alpha hemolytic…
staph epidermis … venous catethers
infective endocarditis
most common staph aureus
damage to which artery in cervial esophagus dissection
The inferior thyroid artery originates from the thyrocervical trunk (left) or subclavian artery (right). It supplies the cervical portion of the esophagu
freidrich ataxia
deg of lateral corticospinal tract ( spastic paralysis)
deg of spinocerebellar tract ( ataxia)
dorsal columns (dec vib sense proprioception)
common cause of death —– HF
Autosomal recessive
fredreich ataxia gene
fraxatin ch 9
mitochondrial dysfunction
most common consequence of pt with right sided IE
pulomary embolism
Bacterial colonization of the heart valves can lead to the formation of thrombi and subsequent bacterial emboli.
he patient’s early-onset coronary heart disease and marfanoid habitus (tall and thin stature with increased arm span, arachnodactyly) in combination with a history of deep vein thromboses (DVTs) and learning disability raise concern
homocystinuria
Fever, pleuritic chest pain, pericardial friction rub (high-pitched scratching sound), and a pericardial and unilateral pleural effusion occurring 3 weeks after an MI
dressler
immune complex-mediated damage (type III hypersensitivity reaction) to the pericardium.
nitrate tolerance
Development of tolerance is a typical side-effect of chronic nitrate therapy. The mechanism underlying nitrate tolerance is not completely understood but is thought to involve decreased sensitivity of the vascular endothelium to nitrates. The most effective strategy to prevent this is intermittent therapy with nitrate-free intervals of at least 8 hours, which would be accomplished by avoiding isosorbide dinitrate at night.
free wall rupure after mi
within 2 weeks
can lead to cardiac tamponade
previous MI is protective
time line for ventricular anneurysm post MI
few weeks to months
interventricular septal rupture
due to macrophages
3-5 days
pt under treatment for afib and heart failure
attempts suicide
abd pain, hyperkalemia, blurry vision
digoxin toxicity
cholinergic = diarrhea vomiting nausea yellow vision
hyperkalemia
BBlockers overdose
verdose would likely cause hypotension, bradycardia, bronchospasm, and hypoglycemia
woman has a pruritic, red-brown rash over the medial ankles, varicose veins, and bilateral lower extremity edema. Her occupation likely requires her to stand for prolonged periods. These findings suggest
stasis dermatitis due to chronic venous insuff
Dermal deposition of hemosiderin is a key feature of stasis dermatitis.
differentiate ulcers caused bby PAD
they are well demarcated
painful
claudication, hair loss on the leg, or nail changes.
pt undergoes cardiac catheterization and 2 weeks later returns with low urinary output
high creatinine levels
mottle purple discoloration of feet and ischemic changes on big toe
cholestrol embolization syndrome
skin description is livedo reticularis due to vessel spasm
very high Cr due to AKI
txt stop anticoag therapy and begin statins
physiological effect of sotalol
BB with K channel blocking ability
decreased conduction through AV node
how do BB lead to decrease in AV node conduction
blocking b1 rec leads to DECREASED sympathetic tone —– decrease in HR
K+ blocking effect of sotalol …. increased myocyte AP duration due to delayed efflux of K+.—— increased ERP and prolonged QT
slow av cond is eveident by increase PR interval on ecg
prolonged repolarization caused in which classes of antiarrythmic drugs
2 and 4
2- BB
4- calcium cb
both act on pacemaker action potention
which class of antiarythmics works by decreased conduction in cardiac myocytes and purkinje fiber
Decreased conduction in cardiac myocytes and Purkinje fibers is the mechanism by which sodium channel blockers (class I antiarrhythmics) function.
mechanism of fibrates
increase LPL activity — breaks down TG
also INCREASE ppar ALPHA (not gamma) activity—- actually it is the activation of this that increases LPL activity
also increases HDL prodcution
leads to gall stone risk
Fibrates are associated with an increased risk of cholesterol gallstones because they inhibit the cytochrome p450 enzyme cholesterol 7-α hydroxylase (↑ cholesterol and ↓ bile acid concentration in bile).
role of PPAR GAMMA
transcription factor that increases the sensitivity to insulin
GLITAZONES
side effects include = weight gain, edema, risk of fracture
how does glucagon work in BB toxicity
Glucagon increases intracellular cAMP by activating adenylate cyclase, which improves cardiac contractility and heart rate while bypassing the beta receptors. It also improves hypoglycemia.
similarities and diff between digoxin and BB toxicities
BOTH CAUSE HYPOTENSION AND BRADYCARDIA
bb- wheezes or brnochospasm , hypoglycemia
digoxin – abdominal problems, blurry vision yellow vision
most common heart malformation in down syndrom
AVSD
atrioventricular septal defects
Recurrent episodes of pain, swelling, and erythema in various locations in a patient with a history of pancreatic cancer are suggestive of
migratory thrombophlebitis
trosseau
which vein courses medial to the medial condyle of the femur
Great saphenous vein
most common vein involved in migratory thrombophlebitis
GSV saphenous
also popliteal vein can be involved but remember its location is in the popliteal fossa not medial to the medial femural condyle
right broncial artery catheter route after entering the femoral artery
thoracic aorta—–right posterior intercostal artery —– right bronchial artery
left bronchial arteries originate from
directly thoracic aorta
internal thoracic artery
supplies the anterior post chest wall
originates from subclavian artery
right bronchial arteries orginate from
interCOSTAL arteries whch are branches of the thoracic aorta
abnormal placement of infundibular septum leads to whcih congenital heart disease
TOF
absent fusion of septum primum and septum secundum
PFO
Elevated pulmonary artery pressure in a 6 hours old new born raises suspicion for
what is the txt for this condition
PPHN persistent pulmonary HTN of newborn
inhaled NO, increases CGMP by ACTIVATING guanyl cyclase and causes vessel dialation without really affecting the systemic resistence
after NO treatment in a baby with PPHN the baby develops tachypnea with blue grey discoloration of lips toes and nails
why is this>
NO treatment can cause oxidation of Fe 2+ to fe 3+ …. oxidized state of iron cannot carry o2
METHEMOGLOBIN basically
side effects of inhaled NO in neonates include platelet dysfunction, pulmonary edema, and the formation of peroxynitrites.
inhibits mitochondrial cytochrome c oxidase
Cyanide poisoning
treated with METHEMOGLOBIN
iron in oxidized state can bind to cyanide and treat the condiiton
african american with isolated HTN DOC
clorthiadone
thiazide
block nacl at DCT
african pt HTN with metabolic syndrome
dihydropyridine CCB
an artery that travels along the external branch of superior laryngeal nerve
superior thyroid artery which is a direct branch of the ECA
indications for a high risk of DVT
recent surgery within 4 weeks
swelling of area
malignancy
pt presents with DVT
lost 7 kg
smoked 1 pack for 25 yeasr
edema of forearm with overlying erythema and a tender cord like structure
duplex shows thrombosis of left basilic and external jugular veins
whats the diagnosis? how to confirm?
history of thrombosis and superficial migratory thrombophlebitis — migratory thrombophlebitis
raises suspicion for a hypercoagulable state
must do CT abdomen to confirm trosseau syndrome due to pancreatic cancer
a drug that prevents voltage gate dependent calcium entry into myocytes used for trating A FIB can have a side effect like?
gingival hyperplasia
nondehydropryridine like verapamil —- rate control
- slow down AV conduction
- reduces ventricular rate
tinnitus can be a SE of which antiarrythmic drug
quinidine I A
cinchonism prolong qt and hypoT
old pt microscopin exam of heart shows brown perinuclear inclusions and isolated deposits of abnormally folded natriuretic peptide
most likely lipoduscin deposits that result from lysosomal oxidation
what are the heart findings in advance age
sigmoid shaped intraventricular septum
increased myocyte size with reduced numbers
deposition of normal transthyretin protein in ventricles
amyloid proteins appear
eosinophilic glassy homogenous deposits
old woman collapses while walking briskly
grade 3 ejection systolic murmur
intensity decreases with hand grip mannv
think aortic stenosis
dystrophic calicfication of valve
what is dystrophic calcification
localized calcification in abnormal /damaged tissue in patients with normal calium levels
which murmurs increase with handgrip test
AR MR VSD
granulomatous nodules on mitral valve are assoc with
RHD
dabigatran mechanism and indications
direct thrombin inhibitor
prophylaxis of thromboembolism
drug indicated in PAD that inhibits platelet aggreg and cuases vasodialation too
cilostazol
PDE 3 inhibitor— increases cAMP
pt has 10 month history of crampy left lower extremity pain that is exacerbated while walking and releived by rest
smokes 1 pack for 40 yeasr
dry and hairless skin over left foot
PAD
intimal plaque in post tibial artery
systemic hyperplastic arteriosclerosis
small vessel disease
in the setting of sever hypertension (180/120)
onion skin due to the intimal response
a drug is prescribed to increase contractility
selectively inhibits an isoenzyme that is responsible for the degradation of cyclic adenosine monophosphate
what is this drug? and SE?
milrinone
PDE 3 inhibitor
inhibits myosin light chain kinase (cannot phosphorylate myosin) —– leads to muscle relaxation
so SE would be hypotension
which condition with chorea (repetitive movemnts) and psychiaric complications leads to early dementia
huntington
what are aschoff bodies composed of
necrotic debris, t cells, plasma cells, and cardiac histiocytes
old pt dies and autopsy done ventricles are normal
microscopic image is shown
yellow brown perinuclear inclusions
normal aging
lipofuscin due to oxidation of phospholipid molecules
deposition of wild type transthyretin is seen in?
senile amyloidis
PLUS CARDIOMEGALY AND VENTRICULAR THICKENING
yellow brown perinuclear inclusions VS brown sarcoplasmic perinuclear granules
1 seen in normal aging due to oxidation of phospholipid molecules
2 seen in hemochromatosis
aortic stenosis due to metastatic calcification can be caused due to which conditions
primary hyperthyroidism
sarcoidosis
multiple myeloma
CKD
splenic infarcts causes include a fib and intravascular hemolysis how will you differentiate between both
so in intravascular hemolysis other signs like anemia, hyperbilirubinema and increase LDH can be seen also shcitocytes on smear
in a fib pt may have increase LDH but not other anemic symptoms
formation of giant cells in the tunica media
giant cell arteritis
what breaks down the fibrous cap of the atheroma
metalloproteinases secreted by inflammatory cells
what is characteristic of Myxomatous degeneration of mitral valve in MVP
derman sulfate
deposition of glycosaminoglycans
65 years old patient has wide pulse pressure and hypertension
165/79
what can be the cause
age>60 means decreased complianvce of arteries
ISOLATED SYSTOLIC HYPT
the handgrip mnnvr increases murmurs of which heart defects
MR AR and VSD
drugs that cause torsade pointes
ABCDE anti IA arrythmatics (quinidine procainamide dysopyradmide) anti IIIA (sotalol ibutilide) antibiotics antipscycotics antidepressant antiemetics
which anti III arythmatic does not lead to torsade pointes but still has long QT has a SE
amiodarone
dyspnea with a high pitched blowing diastolic murmur at right upper sternal border suggests?
aortic regurgitation
what conditon can aortic dissection lead to?
if the dissection reaches the aortic valve ring it can cause regurgitation
dipyridamole
PDE3 inhibitor
causes coronary vasodialation via activation of A2A rec
pt with chest pain is given dipyridamole/ regadenoson and then comes back with ST depression and twave depression
what is the underlying mechanism
coronary steal syndrome
coronary vasodialation causes blood to be shunted towards the healthier heart making the situation worse
young female with BP of 185/125
papilledema and severe headaches
flank bruit
Fibromuscular dysplasia
DO CT or ultrasonography
