5.15 Cardiovascular Ii

Front 1

The RAAS system is able to restore blood pressure in what two ways? (2)

Back 1

1. aldosterone: ↑CO (retains fluid)
2. AT II: ↑TPR (vasocontricts)

Front 2

1. What effects does ANP specifically have on the kidney?

2. What are the L→R shunts in order of decreasing frequency?

Back 2

1. constricts efferent arterioles/dilates afferent arterioles

2. VSD>ASD>PDA

Front 3

1. What is Eisenmenger's syndrome?

2. What is a wide fixed split on cardiac auscultation indicative of?

3. Compare the timing of cyanosis in R→L shunts versus L→R shunts?

Back 3

1. abnormal L→R shunt progresses such that R pressure increases and reverses the shunting (R→L)

2. ASD

3. R→L: early, L→R later (Eisenmenger's)

Front 4

1. What is tetrology of Fallot and what type of shunting is seen in it?

2. What causes transposition of the great vessels and what type of shunting is seen in it?

Back 4

1. PROVe it: P(pulmonary stenosis), R(right V. hypertrophy), O(overriding aorta), V(VSD). This is a R→L shunt

2. failure of aorticopulmonary septum to twist causing R→L shunt

Front 5

1. What type of shunt is persistant ductus arteriotsus?

2. How does a heart look on Xray with tetrology of fallot?

3. What are the two types of aortic coarctation by age?

Back 5

1. R→L shunting

2. boot shaped d/t hypertrophied R. ventricle

3. Infantile: proximal, Adult: distal

Front 6

1. What is "notching of the ribs" associated with and why?

2. "Machine-like" murmer?

3. What types of cardiac malformations are most common in DiGeorge syndrome?

4. What type of cardiac malformation is most common in the offspring of a diabetic mother?

Back 6

1. coarctation of the aorta causes ↑collateral circulation

2. PDA

3. truncal (truncus arteriosus)

4. transposition of the great vessels

Front 7

1. What is a xanthoma?

2. What is Monckeberg arteriosclerosis?

3. What is synonymous with "onion skin" thickening of the arteries?

Back 7

1. plaques/histiocyte filled lipid noduels in the skin

2. ASYMPTOMATIC medial (no intima) calcification of arteries

3. malignant hypertension

Front 8

1. Describe the structure of an atheroma?

2. What tissues get "red infarcts"?

3. What is the most common cause of sudden cardiac death post-MI?

Back 8

1. lipid/macrophage central necrosis with smooth muscle/fibrous cap

2. tissues with dual blood supply (liver or lung)

3. lethal arrhythmia

Front 9

1. What is the cause of unstable
angina?

2. What are the causes of dilated cardiomyopathy?

Back 9

1. plaque has broken free and is re-thrombosing; imminent MI

2. AABCC: alcohol, anthrocyclines beri beri, coxsackie, chagas

Front 10

1. What type of heart dysfunction is seen in the three different types of cardiomyopathies?

2. What cardiomyopathies have an S3 or an S4?

Back 10

1. restrictive/hypertrophic: diastolic dysfunction; dilated: systolic dysfunction

2. S3: dilated, S4: hypertrophic

Front 11

1. Compare what the central and the peripheral chemoreceptors respond to most?

2. How do the peripheral baroreceptors respond to decreased pressure?

Back 11

1. central: pH/CO2, peripheral: pO2

2.↓stretch → ↓firing → ↑in sympathetic response

Front 12

1. Where are the peripheral chemoreceptors location?

2. What is Dressler's syndrome? When does it occur?

Back 12

1. carotid sinus and aortic arch

2. autoimmune mediated fibrinous pericarditis several week after MI

Front 13

1. Describe the appearance of the heart grossly(1) and histologically(2) during the first day following MI.

Back 13

1. gross: mottled/dark, histo: no change before 4hrs, first signs of necrosis after 4 hrs.

Front 14

1. Describe the progression of MI AFTER day 1 with respect to gross appearance, what is happening to the heart cellularly, and what the heart is at risk for? (3)

Back 14

2-4d(hyperemic): intense inflammation/necrosis→risk arrhythmia

5-10(yellow): macs eating tissue/granulation starting→risk rupture

7w(grey): scar completely formed→risk aneurysm

Front 15

1. What are the serum markers for MI from most specific to least specific?

2. Which area of the heart wall is most susceptible to ischemia and why?

Back 15

1. Troponin I>CK-MB>AST

2. subendocardium: furthest from coronary arteries and receive blood by diffusion

Front 16

1. When does Troponin I elevate after MI and when does it recede?

2. Compare transmural and subendocardial MI's on EKG?

Back 16

1. Troponin I: elevates within 4 hours, recedes in 7-10 days

2. Sub: ST depression; Trans: ST elevation + Q wave

Front 17

1. Why does an individual with CHF have orthopnea?

2. Which type of embolus is associated with DIC?

3. What is Virchow's triad?

4. What are Janeway lesions?

Back 17

1. when supine, there is greater venous return making pulmonary edema worse

2. amniotic fluid embolus

3. hypercoag state, endothelial injury, venous stasis

4. erythmatous lesions on palms and soles seen in bacterial endocarditis

Front 18

1. What are the S/S of bacterial endocarditis?

2. Which pathogen is most synonymous with a prosthetic valve?

3. What is the agent which causes Libman-Sacks endocarditis?

Back 18

1. FROMJANE: Fever, Roth's spots, osler nodes, murmur, janeway lesions, anemia, nailbed splinters, emboli

2. s. epidermidis

3. SLE causes LSE (autoimmune)

Front 19

1. What are Roth spots?

2. Compare acute and subacute endocarditis with respect to pathogens, vegetations, and health of patient?

3. Compare the actions of vasodilators and diuretics with respect to afterload and preload?

Back 19

1. round white spots on retina seen in bacterial endocarditis

2. acute: s. aureus, large bulky lesions on normal valves; subacute: s. viridans, small lesions on pathologic valves

3. vasodilators: ↓afterload; diuretics: ↓preload

Front 20

1. What are Osler's nodes?

2. What is marantic endocarditis?

3. Which valve is most often effected by bacterial endocarditis and what is the exception to this?

Back 20

1. tender raised lesions on pads of fingers/toes seen in bacterial endocarditis

2. non-bacterial valvular vegetations d/t hypercoagulable state

3. mitral valve (x. tricuspid in IVDA)

Front 21

1. What is pulsus paradoxus and what condition is it seen in?

2. What condition is associated with a "tree bark" appearance of the aorta?

3. What is an Aschoff body? What condition is it seen in?

Back 21

1. Pulsus paradoxus is a normal decrease in CO during inspiration; it is made worse by cardiac tamponade

2. Tertiary Syphilis

3. Aschoff body is a cardiac granuloma with giant cell. It is seen in Rheumatic Heart disease

Front 22

What are the hypersensitivity reactions? Which ones involve complement*?

Back 22

I: IgE (anaphylactic)
II: Antibody*
III: Immune Complex*
IV: Delayed Th

Front 23

1. What causes serous pericarditis? (2)

2. Most common cardiac tumor in an adult?

Back 23

1. SLE or virus

2. Myxoma

Front 24

1. What causes fibrinous pericarditis? (2)

2. What are the most common metastatic heart tumors? (2)

Back 24

1. MI or uremia

2. lymphoma and melanoma

Front 25

1. What causes hemorrhagic pericarditis? (2)

2. What is the most common cardiac tumor seen in children?

Back 25

1. Tb or malignancy

2. rhabdomyoma

Front 26

1. What is an EKG manifestation of pericarditis?

2. What is Osler-Weber-Rendu syndrome aka? S/S?

Back 26

1. ST elevation in multiple leads (not-MI)

2. Hereditary Hemorrhagic telangectasia; nosebleeds/telangectasias

Front 27

1. What condition is associated with renal angiomyolipomas and cardiac rhabdomyomas?

2. What marker is associated with Wegener's granulomatosis?

Back 27

1. tuberous sclerosis

2. c-ANCA

Front 28

1. What is the triad of Wegener's Granulomatosis?

2. What is Churg-Strauss syndrome?

Back 28

1. necrotizing vasculitis, necrotizing lung granulomas, necrotizing glomerulopathies (ELK)

2. same as microscopic polyangitis but with EOSINOPHILIC ASTHMA

Front 29

1. Describe microscopic polyangitis?

2. Describe the presentation of Sturg-Weber syndrome?

Back 29

1. Same as Wegener's without the necrotizing lung granulomas

2. S-W: Seizure & portWine

Front 30

1. What conditions are associated with p-ANCA? (2)

2. What is Henoch-Schonlein Purpura and the triad associated with it?

Back 30

1. microscopic polyangitis AND Churg-Strauss

2. IgA deposits in vessels of skin, GI, joint, kidneys

Front 31

1. What are the S/S of Kawasaki Disease?

2. What arteries are often affected by polyarteritis nordosa?

3. What arteries are typically effected by giant cell arteritis?

Back 31

1. CRASH a motorcycle: Conjunctivitis, Red Rash, Adenopathy, Strawberry Tongue, Heart (coronary aneurysm)

2. renals/visceral

3. large branches off the carotid (head/face)

Front 32

1. 30% of patients with polyarteritis nordosa have what seropositivity?

2. What is another name for thromboarteritis obliterans? What is it typically caused by?

Back 32

1. HBV

2. Buerger's disease; heavy smokers cause hypercoag w/ clotting and necrosis

Front 33

1. What condition is known as pulseless disease? Who does it typically affect?

2. Who does giant cell arteritis typically effect?

Back 33

1. Takayasu arteritis; asian females

2. Elderly females

Front 34

1. Describe the damage to the arteries in Takayasu's arteritis?

2. What is the treatment for Buerger's disease?

Back 34

1. granulomatous thickening of aorta causes decreased pulses

2. stop smoking

Front 35

1. What part of the vasculature does NO donors typically effect and the effect this has for hemodynamics?

2. What two drugs cause vasodilation via K+ channel opening?

Back 35

1. NO effects the veins → ↓preload

2. minoXidil, diazoXide

Front 36

1. Which drugs are used for hypertensive emergencies? (3)?

Back 36

1. fenoldopam, nitroprusside, diazoxide

Front 37

1. Which lipid lowering agent has the largest positive impact on HDL levels?

Back 37

1. niacin

Front 38

What are the various apolipoproteins and their functions?

Back 38

A-I: Activates LCAT (HDL protein)
B-100: VLDL secretion (also binds LDL)
B-48: Chylo secretion
C-II: LPL Cofactor (HDL lends this to chylo/VLDL)
E: Exit signal for remnant chylo/IDL

Front 39

1. How do aortic arch baroreceptors respond to increased stretch?

Back 39

↑stretch → ↑firing → ↑parasymp/↓symp.

Front 40

1. What nerves relay information from each of the peripher baro/chemoreceptors?

Back 40

1. aortic: CNX, carotid: CNIX