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Flashcards in Uworld Vascular Deck (51):

Where is venous O2 the lowest?

Coronary sinus.This is because heart is very efficient and extracts 90% of O2 out of vesels.Body extracts 75-80% of O2.


When do you begint o see fatty streaks? What are they composed of?

Composed of foamy macrophages . Fatty streaks appear in aortas of childre less than 1 year old. Are present in aorts of all children over 10. May be precursors of atheromatous plaques, but not all fatty streaks progress.


What does the 6th pharyngela ouch form?

Pulmonary arteries and ductus arteriosus.


In INC central central venous pressure, how can one prevent WITHOUT edema?

INC lymphatic drainage.


What heart/vessel drug causes angioedema?What causes peripheral edema + flushing

Angioedema - ACEPeripheral edema + flushing - DHP Ca antagonist (Amlodipine)


Major cuase of AAA?

Atherosclerosis. Start w/ intimal streak. These can proress to atheromas, which weaken underlying meda of aortic wall.


What hemangiomas are common in infancny? In adults?Which regress/dont regress?

Strawberry hemangiomas - children (First few weeks of life) - regress spontaneously at 5-8 years old. Can be found in deep tissue, esp liver. Cherry hemangoas - adults - stay. Frquency INC w/ age.


Anaphylactic Shock. First line. SEcond line?

Epi.Alpha1 - vasoconstrictionB1 - INC contractilityB2 - bronchodilates.Norepi doesnt bronchodilateSecond line - Diphenhydramine - 1st gen antihistamine - use after pt is stabilized w/ epi.


Concern w/ ACE inhibitors? (2)

Angioedema1st dose HYPOTENSION. ESP if there is preexisting diuretic (thiazide/loop) being used.


Central lines -w hich is least likely to get infected? Most likely?

Subclavian vein has lowest risk, then IJV. Femoral has greatest risk. BTW ROUTINE REPLACEMENT OF CENTERAL VENOUS CATEHTERS IS NOT NECESSARY. No evidence that it DEC infection. SHould be remved prompty when no longer required tho. proper Hand washingCHlorhexidien for skin disinfection.Avoid femoralRemove when needed


Describe pathway of fat absorption in body.

Chylomicrons (synthesized in RER/gogli of small intestine enterocyte)Chylomicrons released w/ ONLY ApoB48.HDL give chylomicrons ApoC2 and ApoE.Lipoprotein Lipase activated by ApoC2 on chylomicrons and VLDL. Thus, ApoC2 def -> hyperchylomicronemia.ApoB-100 is present on LDL and required for receptor mediated ptake of LDL by EXTRAhepatic cells.'ApoA-1 - LCAT activation (Cholesterol esterification)ApoE3, E4 - VLDL and chylomicron remnan uptake by liver cells.


Chylomicrons assembly and secretion?Given by HDL to chylomicrons?Activates Lipoprotein lipase?Activates LCAT activation (choletserol esterification?)Causes VLDL chylomicron remnant uptake by liver LDL particle utake by extrahepatic cells?

ApoB48 - chylo assemblyApoC2 and ApoE - given by HDL to chyloApoC2 - Lipoprotein lipase activityApoA-1 - LCAT activationApoE3,E4 - VLDL chylomicron reuptake by LIVERApoB-100 - LDL uptake by EXTRAHEPATIC


Gouty arthritis can be a sign of what drug use?

Niacin. Also facial flushing and warmth. may be prevented by pre-adminsitration of aspririn.Hepatotox w/ high dose nicotininc acid. Nicotininc acid INC HDL by 25-30%.


Cause of INC in staph blood stream infections?

Intravascular devices (indwelling catheters etc)I picked laparoscopic surgeries (thinking epidermitis), but these asa whole have DEC infection from open heart.


Where is COX 2 found?

COX2 is an enzmye that is NOT found in most tissue (only in inflam cells including M!)COX1 on the other hand is fiound in all tisues.


Where/how do:Colchicine act?Infliximab?

Colchicine - binds to tubulin - inhibits microtubule formation - Impairs N! mitosis as well as DEC N! motility.Inflixamab - monoclonal ab that irreversibly binds to TNFa (cytokine).


Niacin - how does it work

DEC hepatic VLDL synthesis!! by DEC FFA release from peripheral tissues.


Pharyngeal arches. GO through all of them123456

1 - Trigeminal nerve (5) + maxillary artery2. Facial nerve (7)+ face muscles3. Glossopharnygeal nerve (9) - internal carotid4. Vagus (10) - subclavian arteries - muscles of pharynx/soft palate - 5. NOTHING. Obliterated6. Recurrent laryngeal branch of vagus. Pulmonary arteries and ductus arteriosus. Most muscles of the larynx.


What are the response sof low dose Dopamine on physio?High Doses?

B1 and D1B1 - INC heart rate/contractility etc.D1 - INC renal blood flow/glomerlar filtration rate, sodium EXCRETION. At high doses, also stimulates a1 receptors - vasoconsrction -> DEC cardiac output due to INC afeterlaod.


What to give those underging hip surgery?When do you use aspirin prophylaxis?When do you use heparin prophylaxis

Aspirin - low dose - prevents coronary artery thrombisis and ischemic strokes. Aspirin is not strong neough to prevent DVT/PE in high risk pt (thos eudnergoing hip surgery) - must give low dose heparin to prevent PE in hospitalized pt.


Small bluish lesion under nail. Painful to touch.2 etiologies?

Melanoma - melanocytes (pigmentation)Glomangioma - tumor of smooth muscle cells of glomus body.GLomus body are found in nail beds, fingers toes, ears. COmpoased of afferent arteriole connectinos to richly innervated muscular AV anastomosis. Shunts blood away from skin surfac ein cold weather and the opposite.


What does C-ANCA and P-ANCA target?

C-ANCA - neutrophil proteinase 3P-ANCA - Neutrophil MPO


If a tumor cell expresses CD31 think?

CD31 means PECAM1 (plateetl ENDOTHELIAL CELL ADHESION MOLECULE) - This is a vascular tumor. Seen in angiosarcoma.


What i THE most likley presentation of hyperchylomicornemia (hypertriglyceridemia)

Ab pain - from acute pancreatitis.Usu not at risk for preamture CAD. Skin xanthomas may be present w/ hypertriglyceridemiaTendon/tubular xanthomas are usu present w/ hypercholesterolemia.


complications of Varicose veins?

Skin ulcerations, poor wound healing, superficila infections.Varicose veins are SUPERFICIAL. Any thromboses is not a DVT and occurs infrequently w/ varicose veins.Get more superficial problem sinstead.


When to be cautious about ACE inhibitors. Why?

Pt w/ renal artery stenosis have a hard time getting blood in.Angiotensin 2 constrictions the efferent arterioles, which allows pt to maintain a GFR> If ACE inhibitors used, can reduce renal perfusion and get acute renal failure. Contraindicated in bilateral renal artery stenosis and unilateral stenosis IF ther eis a solitary functioning kidney.1 good kidney + good artery is fine w/ ACE it sounds like.


Peristend lymphedema pts pt at risk for? THink radical mastectomy w/ right arm sswelling.

Lymphangiosarcoma. Rare enoplasm of endothelial ining of lymphatic channels. Appears approx 10 years following radical mastectomy. NOT Cavernous hemangiomas - benign neoplasms of small vessel endothelial cells. Risk not related to lymphedema.


How is atehrosclerosis initiated?

repetitive endothelial cell injury


What is likelihood of plaque rupture most associated with?

Plaque stability. Not size.Stability depends ont he mechanical strenght of birous cap.Inflam cells in intima may reduce plaque stability by secreting metalloproteinases, which degrade collagen.


Drug combo most likley to cause rhabdo/myositis in cardio patients?

Statin + Fibrate


Norepi extravasation. What is this and how can it be treated?

This means that a1 vasoconstrction of NE has led to local tissue necrosis (cold, hard, pale) - Tx w/ phentolamine - reversible alpha blocker


What do the cardinal veins form?

systemic circulation veinsUmbilical veins ->DegenerateVitelline veins -> portal veinsCardian veins -> systemic circulation


What is age related ISOLATED systolic hypertensino due to?

Seen in 20-30% of ppl 80 and olrder.Due to DEC compliance of aorta (stiffening) and its proximal major branches.


Treatment chart for:Hypercholesterolemia?Hypertriglyeridemia?Low HDL?

Hypercholesterolemia -> Statin -> EzetimibeHyperTG - Fibrates - NiacinLowl HDL -> Niacin


Transmural inflam of arterial wall w/ fibrinoid necrosis think?

Polyarteritis nodosa - no lungs


Segemental vasculitis extending into contiguous veins and nerves think?

Buergers - es w/ nicotinic immune hypersensitivty in heavy smoker (thromboangiitis obliterans) 0 tibial or radial arteries - May see acute and chronic infla, w/ thrombosis of lumen. can extend into veins and nerves - feature RARELY seen in other vasculitis.


Berry aneurism think?

T4 Ehlers Danlos , polycystic kidney diseaseNOT MARFANS.


Histo Description of marfans vascular problem?

Myxomatous change to media -> cystic medial degeneration -> aortic aneurysm


Intermittent claudication think?

Atheroscloersis of arteries (lipid filled intimal plaques)If seen in aortoiliac atherosclerosis -> DEC blood flow to internal pudendal of internal iliac - may be difficult to sustain an erection. Unless this is Temporal Arteritis (claudication of jaw) - in which case granulomatous inflam .PMR. INC ESR>


Intimal thickening - what is this caused by?What stimulates this thickening and other cellular components?

Vascular reaction to endothelial and intimal injury is intimal hyperplasia and fibrosis - from REACTIVE SMOOTH MUSCLE CELLS that migrate from the media to the intima. DO not confuse w/ fibrous plaque, which is fat laden M! etc. PLATELETS STIMULATE THIIS ALL W/ PDGF AND TGFB.


Alpha agonists - if you give, what affect other than INC blood pressure would they have

DEC heart rate (slow AV conduction), contractility, and conductance.INC systemic BP is assoc w/ reflex vagal influence on heart.


What is substance P?

Pain neurotransmitter in both peripehral and CNS. THought to regulate mood, anxiety, and stress behavior in CNSCapsaicin DEC pain by DEC subtance P in peripehral nervous system.


Pathogenesis of atheromas.

1. Endothelial cell injury and INC permeability2. Leukocyte adhesion and altered gene expression. Platelet adhesion and release of Platelet derived growth factor. 3. PDGF -> platelets, M! and promotes migration of SMOOTH MUSCLE CELLS from the media to the intima. Platelets also release TGF-B which is chemotactic for smooth muscel cells. TGFB also induces intestitial collagen production.


What could Rise in serum creatinine in a pt treated for HTN be due to?

ACE. AT2 - constrictions Efferent, INC GFR and Cr excretion.Prevent AT2 creation, you get DILATION of efferent. DEC GFR, INC Cr remaining in body. Also why ACE inhibitors are contraindicated in pt w/ renal artery stenosis.


Formula of TPR in parallel?

1/R + 1/R ... = 1/TPRDOnt forget that last step!


Which artery is favored in CABG? Why?Where do they obtain Saphenous from?

Internal thoracic ARTERY favored - better patency than saphenous. However, for multiple CABG places, saphenous is used due to lenght.It is harvested right at the femoral triangle, just inferolateral to the pubic tubercle.


Homogenous deposition of eosinophilic material in intima and medla of small arteries/arteroles - think which 2 things?

Hyaline arteriolosclerosis -> Nonmalignant HTN or DIABETES.


WHy would an inhibitor of fatty acid oxidation be considered in reatment for angina?

Fat generates more energy.BUT glucose uses oxygen more effectively for energy generation. I guess fat uses a lot of O2 for energy?


What are the 2 major HTN emergency drugs? Describe mech and side effects of both/

Nitroprusside - INC cGMP via direct lease of NO. Can cause cyanide tox (tx/ w thiosulfate)Fenoldopam - DOpamine D1 receptor agonists - causes renal, cornoary, peripheral AVSODILATION. DEC BP and INC natriuresis. This is because D1=D2>B>aB is favored in dopamine


Nasal congestion.Tx - 1 week reliefNasal congestion comes back. Why?

It was alpha agonist being given (phenylephrine etc)These have RAPIDLY DECLING EFFECT after first few days - due to TACHYPHYLAXIS.DEC endogenous NE due to negative feedback, results in relative VASODILATIOn -> edema and congestion. Stop adrenergic agonists to allw for restoration of normal NE feedback pathways. NITROGLYCERINE also has tachyphylaxis. Should have a 8-10 hour drug free period to prevent tachyphylaxis.


How does cyanide treatment work?

Cyanide is toxic, thiocynate is not.So you can give nitrates to convert Hb to metHb, which binds cyanide, then give sulfur (thiosulfate).THIOSULFATE donates Thio to cyanate - soaks it up by forming thiocynate, which is not toxic and can be renally excreted.