Cardiovascular Post 58: (Dated: April 10 - 2009)

Cardiovascular
Post 58: (Dated: April 10 - 2009)

Jugular venous pulse: Its usually on the right side where we examine the pt. The best way of finding out is when systole occurs ---> when 1st heart sound occurs, then you can clearly identify the waves. The C-Wave corresponds with the first Heart sound, which is the begining of systole.

There are 3 positive waves: A, C, V
Two Negative waves: X and Y

A = Rt atrial contraction in late diastole. That is to get the last bit of blood out to fill up that Rt ventrical. When it does that the last contraction, lots of the blood goes into the Rt ventricle, little bit backs up and the venous pulse creates a +ve A-wave. So A-wave due to late atrial contraction and the ventricle.

As the tricuspid valve closes in systole and there is contraction ---> blood goes up to PA, and some of it will hit against the Tricuspid valve and bulge it out a little bit into the Rt atrium ---> Creates a C-Wave.

Make a picture: Systole occured, Rt ventricle contracted and triscup valve is closed and bulge out initially. Blood going right up to PA an creates a little negative pressure behind it and sux the valves down a little bit ---> x-waves which is negative.

V-Wave: Is the filling up of Rt atrium with blood in systole. The tricuspid valve is still closed, systole occuring, blood going out the PA but your Rt atrium has to fill up again. So v-waves actually corresponding with the actual begining of Diastole, the S2 heart sound.

Regular-Irregular Pulse: Its Mitral stenosis ---> A-wave is disappeared, because thats atrial contraction. Whats been discribed here is atrial fibrillation.

If this heart sound was present but usually it is't. What heart sound would be absent? Ans- S4.

It relates to atrial contraction against the increase resistance. So you will have an absent A-Wave if you have A-Fib and if you have S4, you will loose it because it deals with atrial contraction.

Tricuspid stenosis (TS): The atrium had to contract against a valve that did't wanted to open ---> A-wave become huge called Giant A-wave.

Tricuspid regurgitation (TR): Systole occured and lots of blood went into the Rt atrium and some went up to PA --->you will get Giant C-V-wave.

So giant A-wave is TS and giant C-V-wave is TR.

When you have turbidity of plasma ---> its due to only triglyceride not cholesterol.

There are 2 fractions that carry triglycerides:

Chylomicrons from the triglyceride you eat at Mc Donalds which is saturated fat, which are long chain fatty acids and they are being broken down in your gut with the help of lipases and reassembled in small intestine and stuck in chylomicrons. So its exogenous or diet drived triglycerides. In order to find the acurate triglyceride levels thats telling you about the pts real triglyceride level, you must fast for 12 hrs otherwise any kind of fatty food, that would be in chylomicron ---> falsely increase the triglyceride.

You dont fast for an accurate cholesterol and you can go to Mc Donalds if you want ---> get HDL and cholesterol level and it wont be affected by it at all ---> <3% cholesterol present in chylomicrons ---> you dont have to fast to get an accurate cholesterol and HDL (for cholesterol measuring).

But you have to fast to get triglycerides levels because there will be chylomicrons related to the crap that you ate.

What is it called that the triglyceride we make ---> VLDL, what we make in liver from glyerol 3 phosphate which came from glucose and its increased among all alcoholics, because of all that NADH, pushing the DHAP to glycerol 3 phosphate.

VLDL are more dense than chylomicrons because of little protein in it. Chylomicrons hardly have any proteins so it floats.

So you see this kinda white with yellow, its chylomicron. When you see this pinkish turbidity below thats called the Infernate, thats VLDL.

Cardiovascular
Post 59: (Dated: April 12 - 2009)
So a simple tube placed in the refrigerator at 4 degrees and you can tell what lipid fractions are responsible for your elevated triglycerides. So this pt is combination of excess chylomicrons probably because he did't fast and increase in VLDL.

Look at this tube thats perfectly normal. Cholesterol could be elevated but it wont produce turbity.

This one: High chylomicrons, VLDL-none. The pt was't fasting.

What if there was no supernate (chylomicrons) but you have turbit infernate ---> increase in VLDL ---> Type IV hyperlipoproteinemia.

So you fast to decrease the triglycerides derived from diet. We dont need fast, to get accurate cholesterol and HDL.

Slide: Xanthalesma ---> Xanth = Yellow, alesma = Eyelid; Cholesterol causing the yellow ---> you somebody with this get lipid profile. It wont be triglycerides but it would be cholesterol.

Slide: Xanthoma of the Achilles Tendon, in a pt who have a family history of death by coronary artery disease by 20 years of age ---> familial hypercholesterolemia, autosomal dominant disease with absent LDL receptor. Achilles Tendon xanthoma is pathognomonic for that genetic disease.

All that LDL thats supposed to be going into cells cant go there, so it builds up and at 18 you get your first coronary and usually you are dead very shortly thereafter.

Probably at birth they put you on HMG-COA reductase inhibitor, in order to keep yourcholesterol down. They are also doing gene therapy on this, trying to figure out whats the code for LDL receptor ---> they take that code and make a copy and stick into some virus or something to put into the host genome.

Severe combined immunodeficiencies (SCID): They found the code for missing enzyme adenine deaminase. They copied it and stuck in Adeno virus which is a DNA virus ---> they stuck into the genome of that virus ---> they infected the kid with adeno virus ---> virus replicates itself and put its DNA into the host DNA ---> carried along with it the code for adenine deaminase ---> Kid is alive.

Slide: Atherosclerosis in Aorta.

Atherosclerosis: Some thing injuring the endothelial cells lining the elastic arteries andmuscular arteries.

Inurious things: Component of cigarette smoke ---> amonia, CO, and other horrible things that damage the endothelial cells; LDL ---> if oxidized its really bad; Viral infections like clamydia pneumoniae (2nd MCC of atypical pneumonia)---> most of the pts that have MI, most of them had antibodies against C.pneumoniae ---> may be an infection with that atypical clamydia and potentially may be something in it causing vascular damage and predisposing to atherosclerosis; and homocysteine.

When you damage endothelial cells, platelets stick to it. So platelets have PDGF in it and they release that into the artery ---> smooth mucles cells in the media of the vessel ---> starts proliferating, undergo hyperplasia ---> they start chemotactically migrating like a school of fish to the sub-intimal level, they move from media to right underneath the intima of the vessel; The monocytes now have access into the vessels because its been injured, monocytes also have growth factors that do the same thing ---> if you have increase in LDL ---> smooth mucles and macrophages phagocytize the LDL ---> produces the fatty streak.

So its basically, macrophages and smooth muscle cells that have LDL in them that produces the yellowish discoloration. Over time there is an injury that occurs, there is a release of fibroblast that developed in there ---> you end up with a fibrofatty plaque which is the pathognomonic lession of atherosclerosis ---> it can become complicated by dystrophic calfication, fissuring, and thrombosis.

Atherosclerosis: There are lots of cells involved like platelets, monocytes and macrophages, even Cytotoxic T-Cells are involved with cytokines. Not neutrophils.

Its a primary factor for certain diseases like coronary artery disease mainly because ofatherosclerosis we get thrombus; Stroke ---> atherosclerotic plaques; Abdominal aortic aneurysm is purely an atherosclerotic problem with weakening of vessels; non-traumatic amputation of lower extremities, peripheral vascular disease; Mesentric angina, small bowel infarction; renal vascular HTN, atherosclerotic plaque at the begining of renal artery.

Can small vessels like arterioles get hardened? Ans- Yes.

Slide: These are arterioles, they are not normal. This is called hyaline arteriolosclerosis ---> looks like Onion, C.S its called Hyperplastic arteriolosclerosis.

The Lumen is very narrow. When ever we have lots of pink staining stuff with some tissue, we always use the term Hyaline.

Hyaline arteriolosclerosis: its a small vessel disease. Diabetes and HTN produces this kind of small vessel disease but with different mechanisms.

Diabetes is by non-enzymatic glycosylation; Hb-A1c = glycosylated Hb; So glycosylation is glucose attaching to Amino acids and proteins. In terms Hb-A, it is glucose attaching to Amino acids in Hb-A, it means that it gets glycosylated. Hb-A1c levels correlates with 6-8 weeks what your blood glucose levels were. So its the absolute best way of seeing long term glucose management.

So if <6%, you are diabetic ---> you are in normal glucose range.

All the damgage due to diabetes is purely related to glucose and nothing else. So you have two pathologic processes ---> non-enzymatic glycosylation of small blood vessels including cappilaries in kidney, and osmotic damage.

Osmotic damage: Those tissues that contains aldose reductase (lens, pericytes in the retina, schwann cells) ---> convert glucose into sorbitol, which is osmotically active ---> sucks the water into it and those cells die ---> you get cataracts, micro-aneuryms in the eyes because the pericytes are destroyed and they are weakened so the retinal vessels get aneuryms and you get peripheral neuropathy because your shwann cells are destroyed.

Non-enzymatic glycosylation: Causes the BM of the small vessels, becomes permeable to proteins ---> so the proteins in the plasma kinda leaks into the BM and goes into the vessels wall and produces the hyaline change and narrows that lumen; Similarly in non-enzymatic glycosylation of glomerular BM ---> render it permeable to proteins ---> proteins in urine called microalbuminuria, which is the first change that one sees in diabetic nephropathy, a little bit trace amount of albumin that should't be there.

HTN: Does't use that system to produce this disease, it just uses brute (?) force ---> it just drives because of the increase in diastolic pressures ---> it just the proteins right through the BM there and produces that effect.

When we look at the kidneys in HTN, its shrunken and got the cobblestone appearance on the surface ---> because they have hyaline arteriolosclerosis of the little arterioles in the cortex ---> the schemia and basically its just wasting away with fibrosis and atrophy of tissue. So it has a significant component to the pathology of HTN ---> lacunar strokes, with tiny areas of infarction that occured in internal capsular area, its a hyaline arteriolosclerosis problem related to HTN. So much of the pathology of HTN and diabetes are related to that disease.

Slide: Hyperplastic arteriolosclerosis ---> We see this with malignant HTN. blacks > whites, mainly because HTN is more common in blacks than whites. The BP- 240/160, you have papilledema, this is the kinda vessel changes you see in kidney. Mainly its the vessels disease we see in malignant HTN.

Slide: You see Two kidneys, Aorta, bifurcation and you see the aneurym.

Aneurysm: Its an area of out pouching of a vessel due to weakening of a vessel wall.

Whats causing the weakening the vessel wall causing it to out pouch? Ans- Atherosclerosis.

Terms related to Weakening and Outpouching:

In lungs ---> bronchietasis, its due to cystic fibrosis with infection, destruction of elastic tissue. You get out pouching and dilatation of the bronchi.

GI ---> Divertucular disease, you have a weakening and outpouching of mucosa and submucosa through the area of weakening.

Physio: law of Laplace, wall stress increases when radius increases. It means that ones you start dilating it, it does't stops because when you dilate someting and increase the radius ---> increases the wall stress ---> it just keeps on getting. So in other words all aneuryms will rupture, its just a matter of when.

Why its the most common location for aneuryms? Ans- No vasa-vasorum ---> blood supply to the aorta below the renal arteries. So That means that aorta can only get O2 and nutrients from the blood thats in its lumen ---> so the peripheral part furthest from it, gets screwed. So because of the fact that its not getting enough O2 and nutrients, it would be little bit more succeptible to injury, atherosclerosis, weakening of the walls ---> aneurysms.

Dogs have vasa vassorum below the renal arteries ---> never get aneurysms.

Aneurysms: Most common thing is rupture.

Scenario: Sudden onset of severe left flank pain because the aorta is retroperitoneal (so the bleeder is not in the peritoneal cavity but its present in retroperitoneal tissue); Hypotension, because you can put 25% of your blood supply in your retroperitoneum; pulsatile mass on physical exam ---> Those 3 things = rupture of abdominal aortic aneurym.

Aneurysm of the arch of aorta: MCC is tertiary syphilis.

The pathology of syphilis is vasculitis of arterioles, painless chancre.

Painless chancre: CS ---> shows little arterioles surrounded by plasma cells and the lumen of the vessel is totally shut, so its schemic necrosis. In other words its the ischemia of the overlying tissue and under goes the necrosis. Because the nerves are right next to vessels ---> knocks them off too ---> painless.

Cardiovascular
Post 60: (Dated: April 13 - 2009)

All of syphillis is vasculitis. Thats what the treponeme infects ---> small vessels and arterioles. They are infecting the vasavasorum in the arch of aorta. The richest supply of vasa vasorum is in the arch.

So its logical the treponemes will pick it, so what happens is you get End arteritis obliterans ---> obliterating the lumen, ischemia, weakening under systolic pressures ---> looks like a catcher smith?, looks like that you can catch your heart ball in there ---> aneurysm. The aortic valve ring going to stretch ---> Aortic regurgitation murmur.

A murmur gonna occur because of valvular damage, or valve ring is stretched ---> so you can have stretching of the ring and have nothing wrong with the vavlves and have a murmur.

Scenario: The aorta should be closing in diastole. So you pump the blood out ---> stroke volume out, because the aortic valve cant close properly ---> some of the blood gonna drip back. So you gonna have more volume of blood in your Lt ventricle, some one with Aortic regurgitation ---> Frank starling gonna be working, since you strectch cardiac muscles, you increase the force of contraction. So you have a 120 ml of blood in Lt ventricle and get out 80 ml normally. So the E.F is 80/120 = 0.66.

Lets say you have 200 mls of blood in here because of the blood drifting back in ---> Frank starling ---> they get out 100. Actually its not all that efficient because a normal person gets out 80/120 = 0.66; This is a 100/200 = 0.5 ---> the frank starling is not a normal physiologic process, it occurs in pathologic conditions.

So when you have 100 ml of blood coming out of aorta ---> your heads gonna be going like this (?) ---> the mouth shows the uvula pulsating. The nails have underneath pulsating vessels. stethoscope over the femoral artery, press down ---> Duroziez's sign. They have water hammer pulse; All of this because of increased stroke volume coming out related to the fact that there is more blood in the left ventricle; Classics ones of syphillitic aneurysm in the aorta.The left recurrent laryngeal nerve goes around this arch ---> it streches it ---> hoarseness.

Most common complication of aneyrysm ---> rupture.

Slide: This is syphilitic aortitis. This is the dissecting aortic aneurysm.

Article says: The key factor that causing the tear in the aorta is HTN. This imposes stress on the wall of the vessel. There is a weakening of the elastic artery as well ---> elastic tissue fragmentation. Plus there is a cystic medial necrosis, that kinda where glycosaminoglycans mixed together and have muciny crap there, little cystic pockets.

You can almost see the walls of the aorta rubbing on itself and the middle is like nothing in there ---> fragmented elastic tissue ---> little bit of HTN ---> tears.

Cardiovascular
Post 61: (Dated: April 15 - 2009)

Slide: This is where the tear was in this person. This is the aortic valve, the tear is right over here near the arch of vessel. So what happens is, where ever the area of weakness is in the elastic artery, the blood will dissect. In this pt you can see that it was't distally, but its proximally, its out side of the aorta - thats the linning of aorta. Here is blood ---> the paricardial sac attaches to it ---> blood goes into the heart (pericardium) ---> pt dies of cardiac tamponade. This is called a Proximal dissection which happens to be the most common one.

Because of the fact that most of the tears are up in the arched vessel ---> absent pulse; Very common in dissection thats proximal when that dissect close off the lumen of the subclavian artery, usually on the left ---> absent pulse.

Pain: You will have tearing pain, retrosternal, and radiating to back. The pulse on the left diminished vs the one the right. Tropinin -ve, EKG not shows any signs of acute changes. CXR ---> widening of the aortic knob ---> dissecting aortic aneurysm.

CXR: Excess blood in here, you do the chest xray. The diameter of the proximal aorta is gonna be expanded ---> 85% sensitive so its the screening test of choice.

Confirmation: Trans-esophageal ultrasound, and angiography.

Lots of diseases can predispose to dissection.

Slide: This is Marfans syndrome. The height from the pelvic rim to the feet > pelvic rim to the head. Arms span > height. This guy had an appendectomy, this pt already had operation for his dissection.

In marfans which Autosomal dominant, chromosome 15, defect in fibrillin which is the component in elastic tissue ---> lens dislocation, and dissecting aortic aneurysm. The MCC of death in marfans is MV-prolapse or TCV-prolapse ---> sudden death because of conduction defects.

More Causes: Ehler Danlos, defects in collagen ---> the MCC of death Pregnancy: The most common catastrophic disease of aorta in pregnancy ---> dissecting aortic aneurysm ---> because there is twice the plasma volume during pregnancy (2 RBC mass by 1) ---> Hb concentration decrease; Normally all pregnant women have 11.5 as cutoff point for anemia and for non-pregnant women its 12.5 ---> in pregnancy usually its due to dilutional effect of excess of plasma volume.

Excess of plasma volume for 9 months ---> in some women can cause weakening and you get dissections.

Slide: This guy was smoker with primary lung cancer. Now complaining of headache and blurry vision. So you are looking at his retina, he has retinal vein engorgement, its congested ---> superior vana caval syndrome ---> Its usually due to primary lung cancer knocking off the superior vena cava and you get back up of venous blood into the jugular system into the dural sinuses ---> the pt usually dies. Rx with radiation to shrink down the amount of tumor so that they can get some good blood flowing here.

Superior vena caval syndromes confusing with pancoast tumors which are associated with Horner syndrome. SVC syndrome is just knocking off the SVC and nothing to do with horner syndrome.

Slide: This is sturge weber syndrome. Its vascular malformation in the face. This is in the trigeminal distribution. On the same side of brain there is a AV malformation there as well ---> predisposes to bleeding. Also these pts are little bit mentally retarded.

Slide: This is the osler weber rendu disease showing some of the telengectasia in the GI tract.

If you press this end, these little tentacles will go away ---> Spider angiomas; Normal in pregnant women, due hyperestrinism. Other
ther than pregnant women, spider angioma means cirrhosis ---> MCC of cirrhosis is alcohol --->can't metabolize estrogen and it builds up ---> gynecomastia, gonna have warm skin - palmar erythema and gonna have spider angiomas related to hyperestrinism.

Hyperestinism: No metabolism of 17-keto-steroids ---> gonna aromatize those in adipose into estrogen. So there are 2 ways that you get hyperestrenism in cirrhosis.

Qs: How does this looks different from a petechia? Ans- It looks different for one but if you press that in, this would blanch because its an AV-fistula, in other words you are going from arteriole directly to a venule and bypassing capillaries.

Slide: Picture of a child with red lession, B/L white eye reflex, This kid does't have retinoblastoma.

They show you a kid with a red lession on the face. They are gonna say:
A- Surgically removed
E- Leave that alone ---> Yes

Capillary hemangioma ---> leave them alone.

Slide: kaposi's sarcoma, HPV-8.

There is a lession which is only seen in AIDs pts that looks like kaposi's but its due to a bacteria ---> Bacillary angiomatosis due to bartonella henselae ---> seen by Silver stain. Rx with Sulfa drug and it goes away. Also the cause of cat-scratch disease.

Slide: This is a angiosarcoma of the liver. Pneumonic - VAT (Vinyl chloride, Arsenic and thorotrast).

Vinyl chloride: Present in people doing work with plastics and rubber.

Arsenic: Part of pesticides.

Vasculitis: there is a vasculitis of musclar arteries, and elastic arteries just like platelet disorder have different signs symptoms from coagulation disorders.

Small vessel vasculitis: 99% of the time its Type-III HSV, which means it involves immune deposition ---> in small vessel and activates complement C5a, attracts neutrophils ---> fibrinoid necrosis and damage to that small vessel + you will have palpable purpura.

The hand of an old person, not palpable but thats just hemorrhage in skin and there was no inflammatory problem. But if it was palpable ---> it would have been small vessel vasculitis, not a platelet one.

Leukocytoclastic vasculitis - nuclear dust??? ---> they have fibrinoid and they are all immune complex diseases.

Muscular arteries: You get a vasculitis like PAN, wegener's granulomatosis ---> you are gonna get vessel thrombosis, not palpable purpura so you gonna have an infarction.

Kawasaki's disease: In children, they are gonna get coronary artery vasculitis. In fact MCC of MI in children is Kawasaki's disease, because part of the syndrome in addition to the mucocutaneous inflammation, desquamation of skin and lymphadenopathy its coronary artery vasculitis. So when you get a thrombosis in poor little dude got an infarction.

So infarction is what you see with muscular artery vasculitis like PAN, W.Granulomatosis, Kawasaki's.

When you knock off elastic arteries then you start dealing with Arched vessels and you are gonna get pulseless disease thats takayasu arteritis. The vasculitis will block off the lumen of one of the arch vessel ---> you get strokes, because it may knock off the part of internal carotid.

Palpable purpura = small vessel vasculitis Infarction = Muscular vasculitis
Pulseless or stroke = Elastic arteries (far east young lady with absent pulse = Takayasu's arteritis)

Slide: This guy has headache; History ---> It hurts right here doc, i cant see at this side. I have aches and pain all over my body. When I chew it hurts ---> Dx- Temporal arteritis.

Temporal arteritis slide: Its a granulomatous (multinucleated giant cells). It can involve other portions of the artery including the opthalmic branch and produce blindness. Thats sedimentation rate is the only screen from temporal arteritis, its not specific for this but if this is an arteritis (an inflammation), Sed.rate should be elevated but if it was not then you can think about TIA or some other thing; Since screen takes time, to take a biopsy and look for these things and the pt can go blind, so you have to put them on corticosteroid on just history alone.

Cardiovascular
Post 62: (Dated: April 17 - 2009)

Polymyalgia rheumatica: Muscle aches and pains. Commonly associated with this as well. There is no elevation serum CK where as polymyositis is the inflammation of muscle and you have elevated serum CK.

Slide: This pt smoked. Buerger’s disease, also called as thromboangiitis obliterans or smokers disease. Usually males, young, they get digital vessels thrombosis. They get autoinfarction of their fingers and toes. Does't go away usually by quitting smoking.

Story: Stuffy nose ---> look for amputated finger.???

Scenario: 14 year old boy. URTI 1 week ago, presents with polyarthritis, joint pain, hematuria, RBC casts, and palpable purpura of buttocks and lower extremity ---> Dx- henoch schonlein purpura. The most common vasculitis in children. Its an immune-complex, as are all small vessel vasculitides, its an anti-IgA immunecomplex and the RBC cast is glomerulonephritis.

Scenario: This pt with saddle nose deformity and it aint congenital syphillis. Also have problems with sinus infections and problems with URTI, lungs problems with nodular masses and also even a rib??? glomerular disease ---> Dx - Wegener's granulomatosis. MCC of saddle nose deformity in USA. Its a granulomatous inflammation and vasculitis involving U.airways, lungs, kidneys and its an antibody thats associated with it, highly specific antineutrophil cytoplasmic antibody (c-ANCA). TOC: cyclophosphamide ---> C = C (c-ANCA). cyclophosphamide can cause hemorrhagic cystitis and blader cancer. Hemorrhagic cystitis is prevented by Mesna.

Polyarteritis nodosa (PAN): A male dominant disease and involves musclar arteries so infarction is part of this thing. Also have anti-neutrophil cytoplasmic antibody but its p-ANCA. PAN is highly associated with Hbs-Ag.

Scenario: IV drug abuser with chronic Hep.B who has a nodular inflammed mass on the lower extremity, hematuria (kidney infarct). Diagnosis? Ans- PAN.

Slide: This is vessel in Rocky mountain spotted fever. Rickettsial organism infects endothelial cells. The spots are in fact petechia. Unlike other Rikettsial diseases with rash, this starts on extremities and goes to the trunk where as the other ones goes from the trunk to the extremities. The vector is Tick.

Tick borne diseases:

Lyme disease = Borrelia burgdorferi; where as Borrelia recurrentis = relapsing fever with antigenic shifts (means it can shifts in terms of antigenicity).

Spirochetes: Leptospira, also Syphillis, Borrelia, and Treponema pallidium.

Slide: This is a fungus. Its wide angle non-septate. This pt with DKA and there is cerebral abcess related to this fungus. Dx? Ans- mucormycosis.

Strong relation b/w DKA and mucormycosis.

Diabetics commonly have Mucor in their frontal sinuses. So when the pt goes in DKA ---> It starts proliferating and goes right through cribriform plate and they invade the frontal lobes ---> infarct it and infects it with the disease.

Slide: Raynaud's Phenomenon. Many things can do this. Causes include:
Cold reacting antibodies and cold reacting globulins ---> people going outside in cold wheather ---> gets raynaud's, cyanosis of the nose and ears ---> they come inside and it goes away.

Either it can be some kind of IgM cold agglutinin disease or cryoglobulinemia, and Hep-C.

Other diseases that are collagen vascular where the first manifestation often Raynauds. This involves the digital vasculitis and eventually a fibrosis ---> progressive systemic sclerosis or scleroderma and its counter part CREST syndrome.

CREST syndrome: little bit variation of scleroderma and the first manifestation is Raynauds but its a different mechanism. Its a natural vasculitis of the digit and eventually you will fibrose the finger ---> like the smoker got their autoamputation of fingers.

C = 2Cs - calcinosis thats dystrophic calcification and centromere antibody (specific).
R = Raynauds
E = Esophageal dysmotility
S = Sclerodactyly
T = Telengectasias - pinpoint areas of hemorrhage looks like osler weber rendu.

Other causes are due to just vasoconstriction. Its common with people with migraine headache who takes Cafergot types of drugs because migraines thats due to dilatation of vessels ---> the medications cause the vasoconstriction ---> some times you can get Raynauds phenomenon after you take cafergot derivatives; beurger's disease also have raynauds associated with it as well.

So vasoconstriction, vasculitis (scleroderma, CREST), Cold reacting antibodies and globulins is another group of diseases.

HTN: Main organs that HTN affects and most common cause of death in HTN:
1- MI
2- Stroke
3- Renal failure

Essential HTN: highest incidence in HTN in black population. The genetic thing associated with it is Multifactorial inheritance or Polygenic inheritance.

Gout is multiple factorial inheritance.

When you ask people if they have family histroy of a coronary disease they say YES. So the coronary artery disease is mulifactorial.

Multifactorial: Diabetes-II, affective disorder, congenital pyloric stenosis, Essential HTN It means that you have a tendency but not necessarily get it.

So you are black and have family history ---> to prevent it from getting E.HTN ---> cant change the genetics like cant get rid of salts in urine ---> retaining too much salts which is the basic mechanism of E.HTN in black population + old people. But can control 2 things like weight (since there is a direct correlation with HTN) and reduce salt intake + excercise ---> reduces risks for developing HTN because those are the other factors which can produce the disease.

Gout: If there is a family history of Gout. Prevention ---> avoid red meat, and absolutely no alcohol which keeps the purine metabolism down.

Type II diabetes Prevention: Weight ---> lean and mean. When you loose adipose you upregulate insulin receptors synthesis.

Some thing you cant do, that will decrease the chance that you can get the multifactorial inheritance:

HTN: like You retain salt ---> retained in ECF ---> plasma volume increases ---> stroke volume increase. So excess salt which likes to go into smooth muscle cells in peripheral resistance arterioles ---> Na+ enter muscles it opens up certain channels for Ca+, which goes in ---> causes the contraction of smooth muscles ---> peripheral resistance arterioles, constricted.

Since peripheral resistance equals to viscosity / radius to 4th power ---> decrease in radius causes increase in peripheral resistance; We are retaining more blood in our arterial system in diastole while the heart is filling up ---> increase in diastolic pressure.

Rx of choice: in blacks or old people is Hydrochlorothiazide ---> you get rid of salts and water ---> drops BP. In hyperlipidemia we cant use beta blocker or Hydrochlorothiazide because these drugs can produce it so we use ACE-inhibitors.

Its a Low renin type of HTN: Because you have increased plasma volume, thats increased blood flow to the renal artery ---> decreased renin.

Complications: MI, and stroke.

Slide: blood is located in globus palidus, putamen area. Thats where almost all HTN bleeds occurs in the brain. Thats because lenticulo striate vessels which are small little branches from the middle cerebral artery ---> under increased pressures forms aneuryms (charcot bouchard) ---> they rupture; So this is not an infarct but its a hematoma. Its a blood clot right there.

Cardiovascular
Post 63: (Dated: April 18 - 2009)

Not good place to have a blood clot. The neurosurgeon can go to silent areas of the brain and suck these out and improve the prognosis.

Slide: This is kidney. The surface is kinda like pebbly ---> hyaline arteriolosclerosis ---> small vessels disease which is causing the ischemia in that kidney ---> atrophy of tubules, destruction of glumeruli, kidney is shrinking ---> Renal failure eventually; Its 3rd MCC of death in HTN.

LVH is the most common overall abnormality in HTN. Its afterload problem ---> left ventricle contracts against an increase resistance ---> LVH and if its long enough ---> heart failure.

Slide: Its normal heart. On the left we have got hypertrophied heart and on the right we have hypertrophied heart but for different reasons.

If you look at this heart its thick and hypertrophied, its called concentric hypertrophy. Over here we have a dilated and hypertrophied heart ---> it involves work.

It will require a lot of work to contract and push blood against an increased afterload like an stenotic aortic valve, and increase TPR from HTN ---> increase in afterload and gonna produce this kind of hypertrophy (?concentric).

In case of valvular problem and you have excess volume of blood in your ventricles, increased preload ---> gonna increase work (Frank starlings) ---> hypertrophy (?dilated).

Concentric hypertrophy is afterload problem.

Dilatation and hypertrophy ---> volume overload and preload problem.

Things make noises when they close.

Systole: mitral and tricupid valve are closing ---> S1 heart sound. Mitral close before the tricuspid because of the higher pressures.

S2: Aortic and pulmonary valves are closing ---> variation with respiration, thats because the diaphragm goes down and increase the intrathoracic pressure ---> blood is being sucked into the right side of the heart and because of that pulmonic valve gonna close latter then the aortic valve. So P2 (pulmonic component of the second heart sound) separates away from A2 on inspiration and comes back on expiration.

So as the second heart sound has the variation with inspiration. The P2 separates away from A2 because there is more blood coming into the right side of the heart so the valves closes a little bit latter.

S3: It may be normal in someone of 30-35 years of age. Over that its usually pathologic.

S1 - begining of systole
S2 - begining of diastole
S3 - in early diastole ---> its due to blood in diastole thats going into a chamber thats volume overloaded ---> so when diastole was occuring, blood from the left atrium was going into this chamber that was already filled with blood ---> makes turbulance and makes a sound called S3 heart sound. So you only hear the S3 in volume overloaded chamber.

S3 can be from left ventricle is volume overloaded in left heart failure, or in right heart failure you have right ventricle volume overloaded so you can have left sided S3 and right sided S3 heart sound.

Analogy: lots of rivers going into the ocean ---> great turbulance in that area as there is one body of water emptying into large body.

Similarly the ocean is the ventricle with lots of fluid in it and the river is the blood coming in diastole and hits this large mass of fluid and there is turbulance ---> S3.

S4: Its in late diastole. When the atrium is contracting, there is a last bit of blood out in to the ventricles.

S4 sound means there is a problem with compliance. The compliance is a filling term ---> its ability to fill up.

When you have a ventricle this thick and you have left atrium contracting and trying to get blood into a thick ventricle and is non-compliant ---> gonna meet some resistance ---> creates vibration and produces the S4 heart sound. So S4 sound is due to problem with compliance. Left atrium is encountering some problem including that blood in late diastole in to that ventricle that does't wanna fill up any more ---> it can be due to 2 reasons ---> one, its so hypertrophied like or it could't be because its already filled up and it has to put blood in already over filled chamber.

Slide: This is volume overloaded it will have S4; In case of HTN you will have S4; We will have S3 there because it has already volume overloaded but also have S4 because it cant fill up any more.

Analogy: Turkey dinner ---> full tummy ---> apple pie ---> hard to put in stomach which is already filled ---> little vibration there called S4 heart sound.

S3-S4: "budup,budup,budup,budup" gallop rythm thats because they have S1,S2,S3,S4.

Differentiate b/w the left or right ---> breathing.

Breath IN: You breath in ---> suck blood into the right side of the heart. All right sided heart murmurs and abnormal heart sounds ie. S3 and S4 ---> increases in intensity on inspiration on the right side.

Breath Out: When you have positive intrathrocic pressures that are helping the left ventricle push blood out of the heart ---> abnormal Heart sounds and murmurs increases in expiration.

Scenarios: Left, Right or middle. Heart sounds

E.HTN ---> Left
MR ---> Right
MS ---> Middle

Stenosis means problem in opening the valves.

Regurgitation or insufficiency means that there is a problem in closing the valves.

In stenosis murmurs when the vavle is opening, thats when the murmur gonna occur.

For Regurgitation murmur all you have to know when the valve is closing.

Who is opening in systole? Ans- Aortic and Pulmonic valve ---> so the murmurs of AS and PS occur in systole. They have to push the blood through a narrow orifice.

Picture of aortic stenosis: Left ventricle contracts, it encountering some great resistance ---> the intensity of the murmur initially going up ---> "Shhhheeeeeeeeee" pushing pushing pushing ---> goes to a peak and "Shheewww" ---> diamond shape configuration thats why its called an ejection murmur.

Cardiovascular
Post 64: (Dated: May 20th - 2009)

So E.Murmur like Aortic stenoisis has crescendo decrescendo appearance.

Valves heard best:

Aortic valve = Rt second intercoastal space.
Pulmonic valve = Lt second intercoastal space
TCV = Lt parasternal border.
MV = Apex

That does't necessarily means thats where the valve is. Its just where the noise is heard.

Aortic stenosis: You have an Ejection type of murmur in systole. Heard best in the right second intercoastal space. Radiates into the carotids and the murmur intensity increases on expiration and you hear S4.

Pulmonic stenosis: Mainly on the left. Ejection type murmur. Increase on expiration.

Diastole: Stenosis murmurs; Mitral and triscupid valves are opening.

Mitral: Stenosis ---> problem in opening it. Left atrium has problem in opening the MV. This valve does't wanna open, and LA has to get it open to get blood in it ---> its gonna get pretty strong because it has an afterload to deal with ---> gets dilated and hypertrophied; Predisposes to Atrial fibrillation with stasis of blood, thrombus and all kind of things.

The left atrium has to force the blood into the ventricle in a milisecond ---> MV snaps open ---> all that blood that was built up behind ---> gushing in ---> mid diastolic rumble; So you have an opening snap followed by a rumbling sound.

In MS there is a problem in opening the valve ---> you are underfilling the LV ---> no hypertrophy at all since all the work done by LA.

The murmur gonna be heard at apex and will increase in intensity on expiration.

Regurgitation: Problem in closing the valve; in systole Mitral and tricuspids are closing. You certainly dont want the mitral, aortic and pulmonic valve to close on systole ---> you wanna make sure that the blood does't go back in to the atrium. So MV and TCV are closing in systole so if they are incompetent and they cant close properly ---> systole occurs ---> because the MV cant close properly and lets say 30 ml goes back into the LA and 50 ml goes out of the aorta ---> there is even more blood in the LA than normal now.

You just put 30 ml of stroke of the Stroke volume in it + its already been trying to fill up ---> you have excess blood there ---> volume overloaded.

Murmur: Since its the problem in closing the valve ---> gonna be "sheeeeeeewwwwwwwww" ---> as the blood all the way through systole is going through incompetent valve into the LA ---> so its pansystolic murmurs; More of a striaght line; Some times obliterating S1 and S2. (not cresendo decresendo)

So again Apical murmur, pansystolic, S3 and S4 heart sound because we have a problem with compliance as well as volume overload, increases in intensity on expiration.

You can figure out the TCR ---> pansystolic, S3 and S4, left parasternal border, increases in intensity on inspiration.

Scenario: IV drug abuser with fever, pansystolic murmur along the parasternal border, S3 and S4, accentuation of the neck veins. Dx? Ans- Infective endocarditis of TCV. Most common infection of IV drug abuser.

The Murmur and heart sounds increase on inspiration ---> Rt sided.

Changed Scenario: They said that the murmur intensity increased on expiration, it would have been infective endocarditis of MV.

Diastole: Closing of Aortic and pulmonic ---> what you just pump out does't comes back in.

Aortic Regurgitation: You have systole ---> the blood goes out ---> the valves should be closing properly but it does't ---> some blood will be trickling back ---> let say 80 cc went out initially and 30 cc of blood drift back in ---> at the begining of diastole you have volume overloaded chamber and frank starling gonna invalve ---> end diastolic volume gonna be 200 ml which is supposed to be 120 ml.

The murmur of AR is heard after the second heart sound because its not closing and the blood is dripping back in ---> makes a sound, high pitch diastolic blowing murmur right in second intercoastal space ---> increases in intensity on expiration, S3 and S4 heart sounds because its a volume overloaded chamber + all those bounding pulse.

The ant. leaflet of M.V ---> is actually one side of the outflow tract out into the aorta ---> the murmur called Austin flint murmur; When you have AR and you have austin flint murmur ---> you call you cardiac surgeon, thats the time to remove the valve because if you have that murmur then you are significantly dripping back in here, that valve has to be replaced.

Scenarios: Left and Right sided heart failure.

This is section through lungs ---> Lf
Liver ---> Rt
Paroxysmal nocturnal dyspnea ---> Rt

Left Heart Failure: Its forward failure or your left ventricle is failed. It has to push against and after load, it fails; it has to deal with an excess volume it fails; you have so many infarcts that the left ventricle no longer muscle and its fibrous tissue so the contractility is decreased.

Cardiovascular
Post 65: (Dated: May 29 - 2009)

So that means that your EDV gonna increased because you cant get all the blood out or you cant push it out. With that pressure the volume gonna go back in to the LA and back into the Pulmonary Vessels ---> increase the hydrostatic pressure ---> Pulmonary Edema.

When you have chronic LHF ---> you have hemmorhage with alveolar macrophages that phagocytose the RBC ---> rusty colored sputum ---> you do cytology and see Heart failure cells, those are alveolar macrophages that have phagocytose the RBC and its broken down into hemosiderin.

LHF is the diagnosis of symptoms ---> "Doc 'm having trouble in breathing"
RHF is the diagnosis of signs ---> Since its the problem in the RT heart getting blood through the Pulmonary vessels to the left heart. So if it fails ---> blood builts behind it ---> its backward failure ---> hydrostatic pressure will increase in the venous circuit ---> you have neck vein distension; painful hepatomegaly called as Nutmeg liver because the increased pressures in the vena cava gonna be transmitted to the hepatic vein which empties into it and back into the liver into the central vein and you are gonna get the little dots all around it and looks like a Nutmeg.

Most common cause of the congested hepatomegaly is RHF. The increase in hydrostatic pressure also gonna produce pitting edema and possibility of even ascities.

So neck vein distension, hepatomegaly, pitting edema, ascities ---> all right heart failure.

When you lie down and go to sleep ---> you can reasorb upto about a litre fluid from interstitium goes into the venous side of circulation because there is no effective gravity any more ---> little bit of extra blood going into the right heart and into the left heart; if you have left heart failure ---> you have all that excess blood that was't there when you were standing up is now coming back and this left heart is having big time problem to get it out and you have more coming in ---> blood goes back into the lungs ---> windows goes up ---> paroxysmal nocturnal dyspnea.

Cardiovascular
Post 66: (Dated: June 02 - 2009)

Eventually it settles down and you go to sleep this stincky thing happens again. If there is one pillow othropnea its not too bad but if you have to sit up ---> serious left heart failure.

You are imposing gravity. Just placing only one pillow decreases your venous return to the right side of your heart. You put two pillows that decreases even more. You sit up it decreases even more. So pillow orthopnea and PND are signs of LHF not right.

Rx of LHF or RHF ---> best non-pharmacological treatment ---> restrict water and salt.

The king of the Rx of heart failure: Its king because it decreases afterload and decreasespreload at the same time ---> ACE inhibitor ---> decreases preload (decrease in aldosterone, decreases salt and water reabsorbtion) and by blocking ATII you decreases vasoconstrictive effect on PRA so you decreasing the afterload.

Article: People that were on ACE-inhibitors and spironolactone did better than those who were on ACE-inhibitors alone. The reason to that was, aldosterone got elevated again even you are on ACE inhibitor so its not a permanent suppression. So giving aldosterone and ACE inhibitor increases prognosis.

High Output failure (HOF): In Endotoxic shock ---> PRA were dilated, C3a, C5a, Nitric oxide ---> increases venous return in the heart.

Poiseles Law: Viscosity over radius to the 4th power. So if you vasso dilate the PRA ---> decreased TPR ---> more blood comes back to the right heart, left heart has to deal with it ---> you run the risk of high output failure.

Beside septic shock another cause of vassodilatation is thiamine deficiency.

Since the problem in thiamine deficiency is ATP depletion ---> smooth mucle cells in the PRA need ATP ---> decreased ATP ---> vassodilation of the PRA ---> HOF.

Graves disease: Thyroid hormone increases synthesis of Beta receptors in the heart ---> increased in force of contraction ---> there is more blood, systolic pressure are higher ---> HOF.

AV-Fistulas: If you are stabbed in leg ---> develop AV-malformation ---> arterial blood bypassing microcirculation goes directly in the venous circulation ---> blood will be coming faster than normal ---> bruit over the mass, pulsatile, if you press the proximal portion of it the heart rate will slow (branham sign).

Fetal circulation: Baby is not exchanging blood with O2 in our lungs. The Pulmonary vessels in fetus look like they have P.Hyp ---> they are so thick that is extremely hard to get blood through the P.A into the left ventricle. Therefore you need PDA in order to get it out of there.

The O2 in fetus is coming from the chorionic villous dipping into the lake of blood which drives from mommy's spiral arterioles. Its not a good O2 source as lungs. So you need high affinity hemoglobin to able to get O2 ---> HbF which has high affinity for O2. The bad thing is that it does't wanna give it up. This produces tissue Hypoxia so EPO is released ---> 18 gm hemoglobin is present normaly. Newborns have polycythemia.

Therefore HbF has high affinity ---> you have more RBCs with more Hb in it.
Cardiovascular
Post 67: (Dated: July 17 - 2009)

So the blood O2 goes through syncytiotrophoblast of chorionic villous ---> cytotrophoblast ---> myxomatous stroma of the chorionic villous ---> goes into the blood vessels of the chorionic villi ---> umbilical vein which has the highest O2 concentration ---> goes up to liver and there are 2 ways it can go ---> (1) In to hepatic sinusoids, and through hepatic vein and gets dumped into IVC or (2) They can select the ductus venosus and goes into right IVC, ---> Right side of the heart.

Picture this: Foramen ovale is opened. Oxygenated blood is coming up from IVC ---> right atrium ---> foramen ovale ---> left atrium ---> left ventricle ---> aorta.

The SVC blood goes through tricuspid valve ---> right ventricle ---> since pulmonary vessels are too thick, blood goes through the patent ductus arteriosus (kept opened by PGE2 made by placenta, a vasodilator) ---> Right-left-shunt ---> dumped into the aorta.

When the baby is born: baby breaths ---> pulmonary vessels gets opened in milli seconds ---> blood goes through them; Patent ductus begins functionally closing and eventually closes and forms the ligamentum arteriosum.

When the blood goes out the Aorta: it goes into 2 umbilical arteries; there is one umbilical vein. The vessels with the least amount of O2 are the umbilical arteries, where as the most O2 is in the umbilical vein.

If you have left-right-shunt and you have Oxygenated blood going into un-oxygenated blood ---> Step up of O2 saturation on the right side.

If you have right-left-shunt with unoxygenated blood going into left side ---> step down.

The O2 saturation of the blood on the right side of the heart, returning from the body is 75%.

The O2 saturation on the left side is 95%.

Slide ASD: Normally there is a membrane in this portion of the septum. Its not just all muscles going straight up there; Notice the close relationship of aortic valve leaflet in that septum.

The left ventricle is stronger then right ---> direction of shunt is left-right ---> Oxygenated blood dumped into the right ventricle ---> Step up; also its gonna pumped out of the pulmonary artery ---> step up. So you have step up of O2 in the right ventricle and pulmonary artery.

If this is not corrected: Since you are volume overloading the right side of the heart by all this blood coming over here ---> pulmonary arteries have to deal with more blood???---> pulmonary hypertension ---> right ventricle having problem in contracting, get bads ---> hypertrophied ---> risk of reversal of shunt because the right ventricle could become stronger than left ventricle ---> eisenmenger syndrome ---> cyanosis (also called as cyanosis tardive).

Most of the VSD close spontaneously, some need to be patched.

Atrial septal defect: It is normal for the fetus to have patent foramen ovale, but its not normal once they are born. The flow of blood is from left to right as left is always stronger than the right ---> step up in R.A ---> goes from 75-85% ---> step up in R.V ---> step up in P.A.

Difference bw ASD vs VSD: Step up of O2 also in right atrium.

Since there is a volume overloading in the right side of the heart ---> risk for Eisenmenger syndrome.

Also there is a risk of paradoxical embolisation.

If there is a DVT in leg ---> embolized up, the pressures in the right side of the heart are increasing ---> patent foramen ovale ---> embolus goes into right atrium ---> left atrium ---> a venous clot in your arterial system.

Fetal alcohol syndrome: Most commonly has ASD associated with it. 2 out of 1000 kids with Fetal alcohol syndrome have ASD.

Patent ductus arteriosus: Normal in fetus but is't when they are born.

Slide: there is a connection bw aorta and the P.A; Aortic pressures are higher ---> Oxygenated blood goes from left and get dumped in to the PA before it goes into the lungs ---> step up in PA about 80%; Since there is an opening bw these, the blood switching back and forth persistently in diastole ---> pheeeeesshhhhh ooooo pheeeeesshhhhh ooooo pheeeeesshhhhh ooooo ---> machinery murmur ---> gonna hear bw the shoulder blades.

PDA: Left-right-shunt ---> volume overload at the Right side of the heart ---> P.HTN. The shunt will be directed like the fetal one. There will be unoxygenated blood dumping in to the aorta. Since the ductus empties distal to subclavian artery ---> babies gonna have pink on top and blue on the bottom because you are dumping unoxygenated blood below the subclavian artery (differential syanosis).

Cardiovascular
Post 68: (Dated: July 22 - 2009)

Congenital Rubella is associated with patent ductus.

PDA with out any other heart defects dependant on it ---> closed with indomethacin, a potent non-steroidal which inhibits PGE2 ---> PDA start to constrict on its own.

tetralogy of fallot: Most common cyanotic congenital heart disease.
1) Over riding Aorta
2) Membranous septal defect
3) Pulmonic stenosis below the valve.
4) R.V hypertrophy.

The degree of Pulmonic stenosis determines the cyanosis.

Not all babies with TOF have cyanosis. They are called Acyanotic-tetrology; The degree of P.Stenosis is't all that bad. When the right ventricle contracts, there would be lots of blood goes up in P.A and gets oxygenated and much less blood will go and get dumped into left ventricle ---> wont have cyanosis at birth.

In case of very severe stenosis: When right ventricle contracts, very little get up there and most of it will be shunted from right to left ---> step down of O2 in left ventricle may from 95-80% ---> cyanosis.

Cardioprotective groups of shunts: PDA and ASD

ASD: the blood will go from left-right ---> step up

PDA: From aorta-Pulmonary artery ---> some of unoxygenated blood also gets oxygenated ---> pulmonary vein is 95% oxygenated.

Its good to have a PDA and patent foramen ovale in TOF.

Abnormalities in right-left shunting: Polycythemia; risk for infective endocarditis, because you have shunt going from right side going into systemic circulation ---> risk for vegetations spreading to brain, and multiple cerebral abcesses any wherethey want.

All congenital heart diseases have risk for infective endocarditis.

Kartagener's syndrome ---> normal heart on the right side of chest.

Transposition of great vessels: Right atrium is still getting unoxygenated blood; left atrium still getting 95% O2 saturated blood from pulmonary vein; the problem is in the ventricles.

Right ventricle is being emptied by Aorta. Left ventricle is emptied by Pulmonary artery.

So the things thats transposed are venticles while atria are fine. Incompatible with life unless you have shunts.

Three shunts are working: Patent foramen ovale, septal defect and PDA.

Since 95% O2.sat in left atrium ---> thats going from left-right atrium---> step up of O2 in right atrium ---> step up in right ventricle ---> some of it, gonna go out the aorta, some of its gonna go in left ventricle.

Since left ventricle is being emptied by P.A ---> blood goes into lungs to get oxygenated.

The blood wont by 95% saturated but may be 80% ---> cyanosis in these patients.

Coarctation of aorta: Pre means before ductus; Post means after ductus.

Pre-ductal occurs in turner syndrome. Most common congenital disease in turners.

Post-ductal are't present at birth; Actually occurs any time in adult life. Its important to recognize because there is a surgically cause of HTN???

Slide: We have stenosis over here in the aorta. Proximally there is a problem with getting blood through that, you will hear a systolic murmur there which probably be heard between the shoulder blades.

There will be lots of pressure build up proximally and this would dilate the proximal aorta ---> lots of pressure going up to those branched vessels like the subclavian and internal carotids; so the BP in upper extremities gonna be higher and certainly than the lower (limb). There is increased blood flow going into the brain right at the junction where the communicating branches hit the main branch of the cerebral vessels, we have no internal elastic lamina and no smooth muscles ---> its a weak area ---> all of us have potential for developing berry aneurysms and HTN will exacerbate it.

In APKD ---> 20-25% cases develope berry aneurysm; Also increase incidence in essential HTN, coarctation or any cause of HTN can produce the berry aneurysm.

Дата добавления: 2015-11-04