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Flashcards in Blood Vessels Deck (122):

pt with right heart failure and increased central venous pressure (CVP) can prevent edema formation with? not decreased aldosterone because

aldosterone is increased due to renal hypoperfusion and exacerbates edema
instead lymphatic drainage can compensate for moderate CVP elevations


what determines likelihood of plague rupture in acute coronary syndrome

mechanical strength of fibrosis cap,
increased with collagen
decreased with metalloproteinases- degrades collagen, activated during inflammation


which anti-plt drug is used for claudication? name two mech of action, better than which other peripheral arterial disease drug?

-phosphodiesterase inhbitor that causes arterial vasodilation and inhibits plt aggregation, asprin


vascular reaction to endothelial and intimal injury is? mediated by? not fibroblasts because. role of endothelial cells?

intimal hyperplasia and fibrosis
-mediated by smooth muscle migration from media to intima. fibroblasts aren't commonly found in tunica intimal of blood vessels. endothelial cells secrete factors PDGF, fibroblast growth factor, and endothelin-1 that promote SMC migration and proliferation.


niacin is synthesized endogenously from:
-vitamin A

-orotic acid


PAN def, organ rarely involved, organ usually involved

-segmental, transmural necrotizing inflammation of medium to small sized arteries
-lung is rarely involved
-renal artery involvement is most prominent



rare malignant neoplasm of endolethial lining of lymphatic channels
-can be caused by persistent lymphedema


cavernous hemangiomas vs cystic hygroma

-benign neoplasms of small blood vessel endothelial cells
-type of cavernous lymphagioma with endothelium lined lymph spaces beneath epidermis. no luminal blood vessels are present


transmural inflammation with fibrinoid necrosis. symptoms, association.

PAN (polyarteritis nodosa)
-fever, malaise, weight loss, abdominal pain, and melena
-hepatitis B


vasculitis associated with
-antibiotic use (penicillin; type III hypersensitivity)
-hepatitis B

-Buerger's disease and atherosclerosis
-microscopic polyangiitis (aka leukocytoclastic angiitis or hypersensitivity angiitis)


total resistance for a group of vessels arranged in parallel is equal to. arranged in series?

1 divided by the sum of the inverse values for resistance. 1/TPR=1/R +1/R2.
-total sum of resistances Rartery+Rarteriole+Rcapillary+Rvenule+Rvein. good measurement for blood flow to a individual organ not total peripheral resistance


most important steps for prevention of central venous catheter infections. not replacement every 7 days because?

-proper hand washing, full barrier precautions during insertion of central line, chlorhexidine for skin disinfection, avoidance of femoral insertion site, removal of catheter when no longer needed.
-replacement at scheduled intervals has not been found to reduce infection rates


which COX enzyme is normally undetectable in most tissues except during inflammation?

-COX-2 is inducible whereas COX-1 is always on


predinisone vs asprin

aspirin inhibits both COX-1 and COX-2
-predinisone bind to cytosolic receptor which then translocate to nucleus where the expression of anti-inflammatory peptides is upregulated


mech of infilumab

-monoclonal antibody the irreversibly binds to and inhibits tumor necrosis factor alpha, a cytokine involved in the inflammatory process.


in a CT image near the which vertebral level. where is the
renal artery

-if you see renal art and veins think vertebral level L1!
-formed by the union of the right and left common iliac veins at level of L4 and L5. located in from of aorta and to the left
-both right and left renal arteries branch from aorta behind IVC
-aorta is near center in front of vertebral body


lymphedema in lower extremities vs varicose veins

-swelling of dorsum of foot and digits that extends proximally. initially it;s soft and pitting edema and then becomes firm and non-pitting
-due to venous valve malfunction. look for statsis dermatitis (erythemia and scaling wit progressive dermal fibrosis and hyperpigmentation)


white coat syndrome. example of what type of conditioning? what is conditioned stimulus?

patient anxiety exvoked by healthcare workers dressed in white coats. example of classical conditioning
-white coat is conditioned stimulus


osler weber rendu sydrome

hereditary hemorrhagic telangiectasia


tram track calcifications on skill radiograph

struge-weber syndrome


tuberous sclerosis presents with what two major complications



high homocsyteine levels is a high risk for what vessel complicaiton? what is it converted to to avoid this?

-arterial an venous thrombosis
-methionine. methyl-THF transfers a methyl group to homocsyteine (via homocysteine metlytransferase) required B 12 (M-THF give methyl groupt to B12 to make methycobalalamin and then B12 gives methyl group to homocysteine to make methionine)


what do you see at L2. not bifircation of aorta because?

-renal vein joins IVC, and lumen of second part of duodenum (looks like IVC), inferior pole of liver*
-bifurcation occurs at L4. also common iliac veins merge to become IVC at level of L4


which organ extracts oxygen from blood vessels more than in any other tissue in body? what increased cardiac perfusion?

resting will extract up 75-80%
working will extract up to 90%
hypoxia and adenosine accumulation increase cardiac perfusion


-when is cardiac muscle perfused?
-which layer of cardiac muscle is prone to ischemia

-cardiac muscle is perfused during diastole
-endocardium b/c coronary compression is highest due to high contraction force.


key functions of apoliproteins
-Apo E-3 and 4

-LCAT activation (cholesterol esterification)
-chylomicron assembly
-LDL particle uptake by extrahepatic cells
-lipoprotein lipase activation (type 1 hyperlipoproteinemia)
-VLDL and chylomicron remnant uptake by liver cells (type III hyperlipoproteinemia)


what cause mirgration of smooth muscle cells from media into intima and their proliferation? what role do b lympocytes play?

-release of platelet-dervied growth factor form plts, endothelial cells, and macrophages
-produce antibodies to oxidized LDL which localizes to atherosclerotic plaque


describe P-ANCA

perinuclear staining antineutrophil anitbodies
aka antibodies to neutrophil myeloperoxidase


churg strauss syndrome-def, main associations (3). other associations vs allergic bronchopulmonary aspergillosis (ABPA)

-idiopathic systemic vasculitis assocaited with adult onset asthma, eosinophilia, and P-ANCA.
-can also have history of allergy mono or polyneuropathy, pulmonary infiltrates, and paranasal sinus abnormalities
-ABPA can produce asthma like clinical symptoms and also eosinophilia however there is no P-ANCA and usually IgE and IgG antibodies instead


characteristics of anaphylactic shock. treatment?

-vasodilation, increased vascular permeability, and bronchoconstriction
-EPI reverses vasoconstriction (alph 1 stimulation), cardiac contractility (beta 1) and bronchodilation (beta 2)
-use diphenhydramine (inhibits H1 in GI, blood vessels, and repsiratory tract) to treat after stabilizing with EPI


what practice causes most hospital related bacteremias

catheter-related infections.


what do polyarteritis nodosa and leuckocytoclastic vasculitits have in common?

both have segmental fibrinoid necrosis (smudgy eosinophilic deposit) of vessels
-PAN is medium to large sized vessels and lueckocytoplasmic vasculitits (aka microscoplic polyangiitis, microscopic polyarteritis, and hypersensitivity vasculitis) is limited to small vessels


compare and contrast takayasu arteritis and temporal arteritis (aka giant cell arteritis)

both have granulomatous inflammation of media
takayasu involves aorta and proximal aortic arterial branch involvement. females less than 40 yrs. lower BP and pulse in upper extremity compared to lower and cold or numb fingers.
-temporal involves distal carotid artery branch involvement, jaw claudication, older pts > 50


MI in young children

Kawasaki's disease. mostly likely Asian children


complication of giant cell arteritis. how to treat?

blindness due to opthalmic artery occlusion. give prednisone therapy immediately


arteroscleorsis leads to what major blood vessel complication?

-aortic dissection


common complications of varicose veins. not thromboemoblism b/c?

-venous stasis ulcers esp over medial malleolus
-b/c varicose veins are in the superficial venous system. TE occurs with DCT in deep veins


phlegmasia alba dolens

-awful white leg, "milk leg"
-consequence of iliofemoral venous thrombosis occuring in peripartum women. pregnancy predisposes to deep venous thombosis due to pressure of gravid uterus on deep pelvic veins


claudication is

pain and weakness associated with extertion. mc due to artery disease not veins.


-medial band-like calcifications
-homogeneous deposition of hyaline material (acellular thickening) in intima and media of small arteries and arterioles
-onion like concentric thickening of walls in arterioles
-segmental vasculitis extending into contiguous veins and nerves

-Monckeburg's medial calcific stenosis
-Hyaline arteriolosclerosis
-hyperplastic arteriolosclerosis
-thromboangiitis obliterans (Buerger's disease)


insulin and saline causes what metabolic changes vs loop diuretics?

-both cause hypokalemia and increased serum bicarbonate
-insulin and saline decrease serum glucose, osmolality. increases sodium
-loop diuretics decreases sodium and increases osmolality.


describe hypertensive crisis

-persisent diastolic pressure exceeding 130mmHg with acute vascular damage
-retinal hemorrhages, exudates, or papilledema
-hypertensive encephalopathy (HA, irritability, alterations in consciousness)


statins are associated with which two complications?
how are they normally metabolized? name the exception? how can it's metabolism lead to increased risk of complications?

-myopathy and hepatitis
-P-450 3A4
-pravastatin; give to pts who are taking an agent that inhibits cytochrome P-450 3A4
-concomitant administration of drugs that inhibit statin metabolism (i.e macrolides) is associated with increased incidence of statin-induced myopathy and rhadomyolysis which can lead acute renal failure


CYP-450 inducers

-Carbamazepine, phenobarbital, phenytoin, rifampin, griseofulvin
-cimetidine, ciprofloxacin, erythromycin, azole antifungals, grapefruit juice, isoniazid, ritonavir (protease inhibitors)


fenodopam (family, mech, best pt pop to use in)

newer parenteral agent that is classified as a selective dopamine-1 receptor agonist.
-it causes arteriolar dilation and natriuresis leading to decreased systemic vascular resistance and blood pressure reduction.
-only IV agent that improves renal function (use in pts with HTN and concomitant renal insufficiency)


most common causes of spontaneous intracranial hemorrhage

-AVMs, ruptured cerebral aneurysms, or sympathomimetic drug abuse (cocaine)


complications of pts with adult type coarctation of aorta

-commonly die of HTN associated complicaitons
-left ventricular failure, ruptured dissection aortic aneurysm, and intracranial hemorrhage
-also increased risk for ruptured intracranial aneurysms b/c of increased incidence of congenital berry aneurysms of the circle of willis as a well as aortic arch HTN


drug's main primary indication and major complication
-fibric acid derviatives (aka fibrates)
-bile-acid derivatives

-high LDL; hepatitis and myopathy
-low LDL; cutaneous vasodilation, hyperglycemia (acanthosis nigricans), hyperuricemia (gout), hepatitis
-High TG; gallstones, myopathy (worse when combined with statins)
-High LDL; GI upset (worsening diverticulosis) hypertrigyceridemia, malabsorption, vit K malabsorption


mech of action
-bile acid resin

-inhibit conversion of HMG-Coa to mevalonate a cholesterol precursor (increases LDL receptors and uptake of LDL)
-inhibit lipolysis in adipose tissue; reduces hepatic VLDL synthesis
-prevent intestinal absorption of bile acids; liver must use cholesterol to make more
-cholesterol absorption blockers at small intestine brush border
-upregulate LPL; leads to increased TG clearance. activates PPAR alpha to induce HDL synthesis


major cause of AAA (abdominal aortic aneurysm). describe the pathogenesis?

-1st intimal (fatty) streaks composed of intimal lipid filled foam cels. (macs that have engulfed LDL) insudate into intima through an injured leaky endothelium
-this progressively weakens the underlying media or aortic


how can ACE inhibitors lead to acute renal failure

-normally ANG II constricts efferent arteriole to maintain GFR
-ACE inhibitors decrease ANG II leading to dilation of e. arteriole, increased RPF and decreased FF (GPF/RPF).
-pts with renal artery stenosis are dependent on e. arteriole constriction to maintain GFR so be careful not to use ACE inhibitors (enalapril)


DD for red-bluish neoplasm underneath nail bed.

-melanomas responsible for pigmentation
-glomus tumor (gloangioma) originates from modified smooth muscle cells that control thermoregulatory function of dermal glomus bodies


which hypolipidemic agent can increase TGs levels. which is first line treatment for increase TGs

-bile acid binding resins (cholestyramine)
-fibric acid derivatives (gemfibrozil)


statins causes what to increase? not ApoB100 concentration because?

-LDL receptor density to decrease circulating LDL.
-b/c ApoB100 is found in LDL and VLDL. these decrease and so does ApoB100


side effect of doxazosin. uses (2)

-1st does hypotension.
-used to treat BPH and HTN


toxic effects of propranolol

-exacerbate bronchial asthma, peripheral vascular disease, and bradycardia. mask hypoglycemic symptoms of diabetic meds


HTN meds for pts with:
-ostereoporsis and essential HTN
-isolated systolic HTN
-coronary art disease and CHF

-alpha blockers (doxazosin, prazosin)
-ACE inhibitors (ramipril, lisinopril) and ARBs
-hydrocholorthiazide (b/c it increases Ca2+ and isoloated systolic THN)
-amlopidine (Ca2+ blocker)
-beta blockers (metoprolol, atenolol)


side effects of amlodipine

flushing and peripheral edema


what is NE extravasation? how to treat? why not isoproterenol?

-blanching of vein into which NE is being infused together with induration and pallor of the tissues surroung the IV site.
-results in vasconstriction
-avoid tissue necrosis with local injection of an alpha 1 blocking drug like phentolamine
-not isoproterenol b/c beta 2 receptors aren't found in subcutaneous tissue blood vessels


causes dilation of a. renal arteriole?
-constriction of e. renal arteriole?

-PGs (FF stays contant b/c RPF also increases with GFR)
-ANG II (FF increases b/c RPF decreases while GFR increases)
both work to increase GFR


presentation of thromboangiitis obliterans? aka? pt pop? hypersensitivity to?

Buerger's disease
-segmental thrombosing vaculitis extending into contiguous veins and nerves encasing them in fibrous tissue
-heavy smokers, before age 35
-hypersensitivity to tobacco extracts


how to treat pt with
high LDL
high TG
low HDL

-1st line treatment for all of them are diet and exercise; but doesn't work as much for low HDL.
-Statin and if LDL is still high give ezetimibe (watch for myopathy)
-fibrate and if TG is still high give Niacin
-give Niacin (esp pts with familial hypoalphalipoproteinemia)


summary of ABG findings in simple acid base disturbances
-metabolic acidosis
-respiratory acidosis
-metabolic alkalosis
-respiratory alkalosis

-decreased pH, decerased pCO2, decreased HCO3-. compensatory response is immediate with hyperventilation and decreased pCO2
-decreased pH, increased pCO2 and increased or normal HCO3-. compensatory response is delayed. kidneys compensate by retaining HCO3- levels usually >30
-increased pH, increased pCO2 and increased HCO3-. compensatory response is immediate. respiratory compensation with hypoventilation and increased pCO2
-increased pH and decreased pCO2, decrease or normal HCO3- compensatory response is delayed kidneys compensate through HCO3- loss levels are<18


xanthelasmas-type of? gross apperance? microscopic? assocaitions? mc cause?

-type of xanthoma,
-yellowish macules/papules found on the medial eyelids
-dermal accumulation of macs containing cholesterol and TGs
-associated with primary or secondary hyperlipidemia (insulin resistancein DN promotes VLDL) or dsylipidemia
-mc cause LDL receptor abnormality


small vessel disease that presents as
-saddle nose and oliguria, C-ANCA
-skin rash and abdominal pain
-weak upper extremity pulses
-HA and blurred vision
-exertonal calf pain and toe ulcers

-nasal mucosal ulcerations (cause of saddle nose) and glomerulonephritis can be seen in granulomatosis with polyangiitis (Wegner's)
-Henoch-Schonlein pupura (can also see polyarthralgia, young males 3-11)
-Takayasu arteritis (aorta and proximal arches)
-giant cell arteritis (GCA)
-thromboangiitis obilterans and atherosclerosis


how to treat Henoch-Schonlein purpura. age? deposition of what is common?

-usually self limited.
- IgA and C3 so watch carefully for glomerulonephritis and end stage renal disease complications
-seen in young males 3-11


difference b/t type A and B aortic disection

-type A both ascending and descending aorta
-type B just descending aorta


aneurysm is associated with?
dissection is associated with?

-teriatry syphilis causing oblterative endateritis or atherosclerosis


which is a more dangerous combination? statin+ezetimibe or statin+gemfibrozil

-statins and ezetimibe has been reported to cause increased risk of myopathy but is much safer than statin plus fibrate
-statins + fibrate increases risk of myopathy. relase of rhabomyocin can lead to hepatotoxicity


risk of fibric acid derivatives and bile acid resins

cholesterol gallstones due to increased cholesterol concentration in bile


how can pleural effusion lead to V/Q mismatch?

pleural effusion can cause atelectasis


which one relates to affinity

-maximum pharmacodynamic effect
-dose of drug require to produce a given effect
-drugs with a high affinity have a greater potency (lower ED50-dose of drug required to produce one-half of the maximum biological effect)


fatty streaks? meaning if seen in child after 10? meaning if seen in child before 10?

-intimal, lipid fill foam cells (macs and SMCs tht have engulfed lipoproteins)
-earliest lesion of atherosclerosis in all individuals after age 10
-before 10 it does not predict occurrence or location of atheromatous plaque later in life


drugs that can cause hyperkalemia/ mech

-nonselective beta-adrenergic blockers (interfere with beat-2 mediated intracellular uptake)
-ACE-inhibitors (inhibit ACE II with decrease in ALD secretion)
-ANGII receptor blockers (blocks AT1r decreasing ALD secretion)
-K+ sparing diuretics (block ENaC (amiloride and triamterene) or ALD receptor (spironolactone and eplerenone))
-cardiac glycosides (i.e digoxin). inhibit Na+/K+ ATPase pump
-NSAIDs (impaired PGs synthesis and decreased renin and ALD secretion)


associated with increased incidence of thromboembolic stroke?

-stroke caused by DVT
-atrial or ventricular septal defect and late onset right to left shunting


what molecule reduces pain by decreasing levels of substance P in peripheral nervous system



cause of flushing induced by niacin? vanc?

-PGs, why it can be inhibited by NSAIDS
-histamine release


alpha 1 receptor activation leads to what changes in BP and HR?

-direct action is to increase systolic and diastolic BP due to vasconstriction
-this leads to reflex increase in vagal tone leading to decreased HR and slower AV node conduction velocity


differences between alpha1 and alpha 2 mediated effects

-alpha 1= contraction of most vascular SM, contraction of pupillary dilator muscle (mydriasis), increased cardiac contractility (not clinically significant due to reflexive vagal tone), increased internal and urethral sphincter tone and increased prostate contraction in men, pilomotor SM contraction
-alpha 2= CNS mediate decrease in BP, decreased aqueous humor fluid production from ciliary body, inhibition of lipolysis in fat cell, inhibition of adrengeric and cholinergic neurotransmitter release
-increased plt aggregation


how to prevent PE caused by DVT. not aspirin b/c?

-prevents plt aggregation to prevent recurrent coronary art thrombosis and ischemic strokes but can't prevent DVT in high risk pts


mech of angioedema secondary to ACE inhibitors

-rare complication
-due to increased bradykinin levels (potent vasodilator)



aka hives
caused by mast cell degranulation


equation for flow?
how does radius affect the two?

-Flow(Q)=P1-P2/ resistance
so now flow (Q)=(P1-P2/nL) *r^4
-blood flow is directly related to radius raised to the 4th power
-resistance is inversely related to the vessel radius raised to the 4th power


NE effect on sympathomimetics receptors
-alpha 1
-alpha 2
-beta 1
-beta 2*

-increased IP3/DAG; peripheral vasodilation
-decreased cAMP, decrease release of NE and insulin
-increased cAMP; increased contractility. however not seen clinically b/c of a reflex bradycardia due to increase in peripheral resistance
-increased cAMP; bronchodilation, but effect is small


name drugs that act on
-beta 1
-beta 2
-dopamines and beta/alpha

-phenylephrine (pure alpha 1>2) and NE (alpha more than beta)
-isoproterenol (pure beta 1=2), EPI (beta more than alpha) unless at high doses then alpha>beta-prob due to reflex brady
-dobutamine (beta 1>beta 2)
-albuterol, salmeterol, and terbutaline (beta2>beta 1)
-dopamine (1=2, beta>alphas)


CD31 aka. tumor marker for? other associations?

-hepatic angiosarcoma
-also associated with arsenic, thorotrast, and polyvinyl chloride


-cherry hemangiomas aka
-strawberry hemangiomas aka
-spider angiomas
-cavernous hemangiomas

senile hemangiomas
-small red, cutaneous papules common in aging adults. do not regress spontaneously and typically increase with age. light micro show proliferation of capillaries and post-capillary venules in papillary dermis (separated by connective tissue).
-infantile/capillary hemangiomas. appear during 1st weeks of life. grow rapidly and then regress at 5-8yrs.
-blanch with pressure and refill with release. bright red papule with several outwardly radiating vessels, are estrogen dependent
-dilated vascular spaces wit thin walled endothelial cel. soft blue, compressible mass. can be on skin mucosa, deep tissues and viscera. don't regress spontaneously like capillary hemangiomas.


cavernous hemagiomas in brain and viscera

von-hippel-lindau disease


drug to give in HTN emergency. how is it metabolized? how is this related to it's toxicity? how to treat overdose?

-nitroprusside, quick onset and short duration
-metabolized to cyanid with conversion to thiocyanate by liver rhodanase
-risk of cyanide toxicity
-sodium thiosulfate (donates sulfur to liver rhodanase to enhances conversion of cyanide to thiocyanate) can also give hydroxocobalamin


migratory thrombophlebitis=

aka Trousseau's syndrome
think CANCER causing hypercoagulable state (visceral like adenocarcinoma of pancreas)


presentation of granulomatosis with polyagiitis (Wegner's)? antibodies are formed against?

-necrotizing vasculitis of the upper and lower respiratory tracks (nasal ulcerations, sinusitis, hemopytsis) and rapidly progressive glomerulonephritis
-neutrophils. C-ANCAs target neutrophil proteinase 3


explain tachyphylaxis

aka rebound rhinorrhea.
topical preparations of alpha agonist cause vasoconstriction of nasal mucosa vessels and are used as a decongestants. overuse of these drugs cause negative feedback, resulting in decreased NE synthesis and release from nerve endings, which diminished their effect


effect of systolic BP, diastolic BP, HR, contractility, and renal blood flood
-Dopamine (low dose)

-beta>alpha. in SBP, decrease DBP, increase HR, increase contractility (beta) and decrease RBP (alpha)
-alpha1>alpha 2. increase SBP, increase DBP, decrease HR. no change in contractility. decrease RBP
-dopamine>beta>alpha. SBP increases, DBP no change, HR increases. contractility increases and RBF increases (dopa dilates renal vasulature)


dopamine doses

-vasodilation (dopamine)
-contractility (beta)
-vasconstriction (alpha)


ways to block RAS?

-beta blocker (prevent renin release from juxtaglomerular cells) decreases all factors .no change on bradykinin b/c ACE activity is not affected
-block AT-1 receptors (ARBS i.e losartan) increases all factors(due to removal of negative feedback). no change in bradykinin b/c ACE activity is not affected
-ACE inhibitors (ramipril). increased renin and ANG I, decreased ALD. incerased bradykinin b/c ACE is responsible for its breakdown


decrescendo-type murrmur over left sternal border

-aortic regurg
can be syphillus, vasa vasorum endarteritis causing aneurysm


avoid ACE inhibitors in which pt pop

renal art stenosis


marker one sided kidney atrophy? pt pop? PE findings?

renal artery stenosis
-occurs in elderly individuals due to atherosclerotic changes in arterial intima or in women of childbearing age due to fibromuscular dysplasia
-HTN and abdominal bruit are present


drugs that myopathy

fibrates, niacin, hydroxychloroquine, glucocorticoids, colchicine, interferon alpha, and penicilamine


-eosinophilic hyaline material in the intima
-onion-like concentric thickening of the walls of arterioles

-hyaline arteriolosclerosis caused by nonmalignant HTN or diabetes
-hyperplastic arteriolosclerosis due to malignant HTN


amiloride vs amlodipine

-diuretic vs Ca2+ blocker


treatment for Conn's syndrome. toxicities

-spironolactone and eplerenone


how do bile acid resins (give example) increase hepatic cholesterol synthesis? how do you block this effect?

-binding bile acids in GI tract. causing increased bile synthesis in liver the synthesis of bile acids requires cholesterol and the decreased cholesterol causes is an activating factor for HMG-CoA reductase to increase cholesterol synthesis.
-block this effect with statins


presentation of hyperTG vs hypercholesterolemia? mech of both

-hyperTG is due to lipoprotein lipase deficiency (responsible for TG clearance). presents as abdominal pain (pancreatitis), eruptive SKIN xanthomas (small yellowish papules surrounded by erythema)
-hypercholesterolemia is due to defect in LDL receptor. increased risk for premature coronary heart disease (chest pain), TUBULAR/TENDON xanthomas (nodular deposits in tendons and xanthelasmas esp in Achilles and elbow)


mech of fatty oxidation inhibitors. why are they useful in pts with stable angina. not more oxygen extraction per minute because?

-newer agents that inhibit fatty acid oxidation and shift energy production to glucose oxidation thus promoting oxygen efficiency. (fatty acid oxidation uses way more Oxy to make energy than glucose oxidation and glycolysis)
-This decreases oxygen needed to support cardiac function and toxic fatty acid metabolic production
-increasing oxy extraction is of little benefit b/c heart already relies heavily on removing large amts of oxy from blood 75%. there's little room left to extract more.


define false aneurysm-complicaiton? two associations.

-aka pseudoaneurysm. breach of all three layers of blood vessel or heart. causes blood leakage within sac of connective tissue surrounding point of arterial wall rupture
-associated with leaks in sites of vascular grafts and post infarction myocardial ruptures


myxomatous changes in media of large arteries. if in younger pts think?

-cystic medial degeneration.
-can cause aortic dissections and aortic aneurysms


ingestion of beta-aminiopropionnitrile can lead to what? found in what types of foods?

-certain types of sweat peas
-mimics myxomatous degeneration can lead to aortic aneurysm


growth pattern of strawberry type capillary hemangiomas? regress when?

-initially they grow in proportion to growth of child and regress usually by age 7


compare and contrast nifedipine/amilodipine vs verapamil

-all are Ca2+ channel blockers
-n and a are selective for vascular smooth muscle
-v is selective for heart (think v=ventricle)


volume of distribution=
low Vd=?
medium Vd
high Vd

amt of drug given (mg)/plasma concentration (mg/L)
-3-5L; stuck in blood or plasma, drug is large/charged/bound to protein
-14L; stuck in ECF. drug is small hydrophilic molecule
-42L; in all tissues including fat. small lipophilic molecules, bound to tissue protein.


is bioavailability related to Vd?

no it's not. instead it's a measure of the absorption of a drug


what is filtration coefficient depend on

Kf depends on area of capillary available for the diffusion and on permeability of capillary membrane
-not needed to calculate net filtration pressue but net fluid movement in a given area in ml/min


what are hydrochlorothiazides contraindicated?

-can elevate glucose (diabetics), hyperlipidemia, uric acid (gout), pts with hypercalemia


risk of nonselective beta blockers and ACE inhibitors. not seen with selective beta 1 blockers because

hyperkalemia- b/c beta 2 causes insulin release and blocking decreases insulin which increases K efflux


name some concerns before starting a pt on ACE inhibitors with low BP? how do you prevent complications?

-1st dose HTN
-risk factors include hyponatremia, hypovolemia secondary to diuretics, high renin levels or high ALD levels, renal impairment and CHF.
-prevent this by identifying pts at risk, initiating therapy at low dosages and follow with cautious dosage titration and BP monitoring


during continuous infusion of a drug metabolized by 1st order kinetics the steady state concentration is reacheed

in 4-5 half lifes


which drugs need to be adjusted with niacin use?

-niacin can potentiate anti-HTN meds b/c of dilatory effects (PGs release). so anti-HTN should decrease
-also niacin can cause insulin resistance (acanthosis nigricans) and necessitates an increase in diabetic meds


epi effect on
DBP (low and high doses)

-increased (dose dependent); beta 1 receptor
-increased (beta 1 and alpha 1)
-low dose decreased (beta 2? alpha 1)
-high dose increased (alpha 1 ?beta 2)


pretreatment of propranolol before epi causes

-blocked beta effects (vasodilation and tachycardia)
-this leaves only the alpha effect (vasoconstriction)


unilateral atrophy of kidney alone
unlateral atrophy of kidney + HTN
-bilateral atrophy of kidney
-bilateral kidney dsyplasia

-congenital renal hypoplasia
-renal artery stenosis (causes oxygen and nutrient depletion)
-aging associated with loss of nephron mass due to arteriolosclerosis (senile changes)
-trophic hormone deficiency


does unilateral denervation of kidney have effect on kidney growth or morphology?