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119 Cards in this Set
- Front
- Back
What marker of inflammation produced by the liver and within atherosclerotic plaques is a strong predictor of MI risk?
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-C-reactive protein (CPR)
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What is the classic presentation of a syringomyelia?
Malformation associated with syringomylia?- |
bilateria loss of pain and temp sensation and potentially weakness and atrophy of hand muscles
chiari malformation- |
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young woman after car accident feels fine but later loses consciousness. CT scan reveals intracranial hemorrhage that does not cross suture lines.
Which bone and vessel were injured in the crash?- |
Classic epidural hematoma
middle-meningeal artery injury caused by injury to temporal bone- |
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Outline pathway by which the heart tube forms the atria of the four-chambered heart.
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. tube grows. elongates, folds into S-shape --> atrial chamber lays posteriorly in S & ventricular chamber lays anteriorly in S; . Atrial chamber grows, incorp. superior vena cava & pulm. vein; . Septum primum forms; . Septum secundum forms incompletely (hole called foramen oval);. Cell death in septum primum forms hole called osmium secundum
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What divides the right ad left atria?
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Septum primum and septum secundum
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How blood shunted from right to left atrium in embryo?
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Through the foramen oval (of the septum secundum) and osmium secundum (of the septum primum)
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3 possible causes of atrial septal defect?
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ostium secundum overlaps foramen ovale
absence of septum secodum neither septum secundum or septum primum develop |
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What structure grows to close the opening/canal between the atrial chamber and ventricle chamber into two smaller openings?
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superior and inferior endocardial cushion
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What genetic abnormality is common with endocardial cushion defects?
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Trisomy 21!!!
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Outline pathway by which ventricles and their outflow tracts are separated
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.Ventricular chamber lays anteriorly in the S-shaped heart tube-->muscular ventricular septum forms which begins to divide the ventricles
.Truncoconical swellings (ridges) of truncus atriosus meet, fuse, zip (both superiorly and inferiorly) in 180 degree turn to form the spiral septum (AKA aorticopulmonary septum) . Inferior portion of spiral septum meets with muscular ventricular septum to divide ventricles and forms the aorta and pulmonary arteries |
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Name & different truncoconical (spiral) septum defects?
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Tetralogy of Fallot
Persistent truncus arteriosus Transposition of the great vessels(RV-->aorta,LV-->PA Dextrocardia Ventricular septal defect (VSD) Fenestrae |
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Describe how the ventricles are remodeled in order to form the atrioventricular valves....
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Myocardium erodes-->ventricles enlarge as a result-->residual mesodermal tissue becomes and forms chord tendinae
Formation of papillary muscles and AV valves |
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Which embryologist structure of the heart gives rise to each of:
Ascending aorta & pulmonary trunk Coronary sinus SVC Smooth parts of L. and R. ventricles smooth part of the right atrium trabeculated left and right atria trabeculated parts of the left and right ventricles |
truncus ateriosus
left horn of sinus venous right common carotid vein & right anterior cardinal vein bulbus cordis right horn of SV primitive atria primitive ventricle |
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What structure divides the truncus arteriosus into the aortic and pulmonary trunks? What is cellular origin of this structure?
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Spiral (aorticopulmonary) septum
derived from neural crest |
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Which fetal vessel has the highest oxygenation?
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umbical vein-->ductus venosus-->IVC-->Right atrium
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What causes the ductus arterioles to close?
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increase in oxygenated blood in aorta-->decreased prostaglandins
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What causes the foramen oval to close?
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infant takes breath-->decreased intrathoracic pressure-->decreased plum vascular resistance-->blood sucked into PA from right atrium-->increased left atrial pressure-->pushing of septumprimum up against septum secundum
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What cell types are rich in smooth ER
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hepatocytes
steroid hormone producing cells of adrenal cortex |
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What are treatments for overdose of heparin & warfarin?
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Warfarin -- FFP & Vitamin K
Heparin -- protamine sulfate |
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Outline pathway for the generation of norepinephrine from tyrosine
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Phenylalanine-->tyrosine - (tyrosine hydroxylase) -->Dopa -(dopamine hydroxylase) -->Dopamine -->NE --> Epi
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Ebstein anomaly
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. tricuspid leaflets are displaced into right ventricle, hypoplastic right ventricle, tricuspid regurg or stenosis
. 80% have a patent foramen oval with right-to-left shunt .dilated right atrium causing increased risk of SVT & WPW . physical exam; widely split S2, tricuspid regurgitation .Associated with maternal lithium |
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What is the most common congenital cardiac anomaly?
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VSD
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What are the components of the tetralogy of Fallot?
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Pulmonary stenosis
Right ventricular hypertrophy Overriding aorta VSD |
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Explain how the great vessels are attached in a transposition of the great vessels
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Aorta attached to Right Ventricle
PA attached to Left to Left ventricle |
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A 45-yr-old man presents with a BP of 160/90 on right arm and 170 on left arm. No palpable pulses in feet/ankle. What problem does the patient most likely have?
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Coarctation of the aorta
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Describe blood flow through a PDA
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Blood flows from aorta into PA due to a left-to-right shunt (after birth)
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Heart defect associated with each of the following disorders?
Chromosome 22q11 deletions down syndrome congenital rubella turner syndrome marfan syndrome |
truncus arteriosis, tetralogy of fallout
endocardial cushion defect --> ASD, VSD PDA, pulm artery stenosis Coarctation in infants, bicuspid aortic valve Aortic insufficiency & dissection |
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Rapid Fire Facts:
Continuous machinery-like murmur "Boot-shaped heart" Rib notching Most common congenital cardiac anomaly Most common congenital cause of early cyanosis |
PDA
Tetralogy of fallout, RVH (in adult) Coarctation of aorta VSD Tetralogy of fallout |
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Type of collagen used in "slippery" tissues? Which is used in "bloody" tissues?
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Collagen Type II -- slippery (cartiliage, vitreous body, nucleus pulposis)
Collegen type III -- bloody (blood vessels, granulations tissue, skin, uterus, fetal tissue) |
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Enzymes used in the catabolism of norepinephrine?
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COMT (catecol-O-methyltransferase)
MAO (monoamine oxidase) |
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What are various clinical applications of atropine?
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decrease airway secretions, pupillary dilation and cycloplegia, decr stomach acid secretion, decr gut mobility, decr urgency, treat bradycardia
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What is the pulse pressure in a patient with systolic blood pressure of 150 mmHg and a mean arterial pressure (MAP) of 90 mm Hg
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PP= systolic = 150-60 = 90 mm Hg
MAP = 2/3 diastolic + 1/3 systolic so, 2/3 diastolic = 90-50 = 40 mm Hg |
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What is the basis equation for cardiac output (CO)? What is the Fick principle?
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CO = SVx HR
CO = rate of O2 consumption/arterial O2 content - Venous 02 content |
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How can the myocardial oxygen demand be decreased in circumstances where the heart is ischemic?
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Decrease after load
Decrease contractibility Decrease HR |
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What can make the stroke volume increase for a given preload?
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increased contractility from:
sympathetic stimulation, ionotropic drugs (catecholamines, digoxin), increased intracellular CA, Decreasing extracellular NA |
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What factors affect stroke volume (SV)?
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--preload (inc with exercise, pregnancy, transfusions and decrease with nitrates (vasodilators)
--afterload (squatting increases and ACE 1 decrease) --contractility (increased by digoxin, catecholamines, decr by HF, acidosis, hypoxia, beta-Ca channel blockers like verapamil) |
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What is the heart ejection faction (EF) ?
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EF = SV/EDV
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Where does each of the following spinal tracts decussate/cross over?
Dorsal columns Lateral corticospinal tract Spinothalmic tract |
medulle
medullary pyramids anterior white commisure |
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What drugs are known for inhabiting cytochrome P450?
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CRACK AMIGOS
Cimetidine, Ritonavir, amniodarone, ciprofloxin, ketoconazole, acute alcohol use, macrolides, imeprizole, grapefruit juice, omeprazole, sulfonamides |
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What is a disulfiram-like reaction? What drugs cause a disulfiram-like reaction?
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Feeling of being hung-over because acetaldehyde dehydrogenase has been inhibited leading to accumulation of aldehyde --flusing, sweating, nausea, headache, hypotension
Metronidazole, certain cephalosporins (cefotetan, cefamadole, cefoperazone), 1st gen sulfonylureas (tolbutaminde) |
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What are the signs of right-sided heart failure?
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Peripheral edema, nutmeg liver, jugular venous distention
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What are the signs of left-sided heart failure?
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Pulmonary edema, crackles, dyspnea on exertion, orthopnea, paroxysmal, nocturnal dyspnea
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How does poor cardiac output result in an increase of aldosterone?
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JG cells sense low BP from low CO -->increase in renin secretion -->converts angiotensinogen to Ang 1 -->Ang II (via ACE) --> aldosterone
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What are the sup toms of organophosphate poisoning? What are the symptoms of atropine overdose?
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muscarinic excess (miosis, urination, diarrhea, bronchospasm, bradycardia, excitation of skeletal muscle and CNS), lacrimation sweating, salvation, abdominal cramping
Atropine: decreased secretions, elevated temp, confusion, disorientation, constipation, urinary retention, cycoplegia and mydriasis |
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Outline the pathway b y which stimulation of a Gq receptor activates protein kinase C
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Gq -->PLC-->PIP2 to IP3 and DAG --> Ca release from (IP3) and PKC (from DAG)
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With what type of congenital heart defect would increasing afterload be beneficial?
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in a right to left shunt (like Tetralogy of fallout, transposition of great vessels, truncus arterioles, or eisenmenger syndrome with VSD, ASD or PDA)
squatting increases after load |
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A 76 year-old Caucasian man who is a competitive bodybuilder comes to the physician complaining that he has started "getting anaerobic" very quickly when exercising. Upon further questioning, you determine that he is experiencing shortness of breath after only 2 to 3 minutes of exercise. Physical exam shows mild pedal edema. Lungs clear. ECG shows est. left ventricular ejection fraction of 25 % without valvular dysfunction. What are the mechanism of action of the drug classes proven to reduce mortality in this patient?
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.
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Which classes of drugs are proven to improve survival and reduce hospitalizations in chronic CHF? Which are used only for symptomatic relief?
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Improved survival: ACE inhibitors, ARBs, Aldosterone antagonists, certain B-blockers (metroprolol, carvedilol, bispolol, (nitrates and hydalazine in some pts)
Symptomatic Relief: Diuretics, Digoxin (incr cardiac output) Vasodilators (prevent pulmonary symptoms) |
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Treatment of ACUTE CHF -
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('NO LIP" --Nitrates, Oxygen, Loop Diuretics, ionotropic drugs, positioning (sit the up)
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Cardiac Clycosides (Digoxin)
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Used for chronic CHF and sometimes to control HR in A-fib
Big diagram! |
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What medications are used to treat chronic heart failure?
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Reduce mortality: ACE 1, ARBs, Aldosterone Antagonists, B-blockers
Improve symptoms: Digoxin, diuretics, vasodilators |
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What medications are used to treat acute heart failure?
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NO LIP
Nitrates, Oxygen, Loop diuretics, lonotropes, positioning (sit pt up) |
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What is the mechanism of action of the cardiac glycosides (e.g., digoxin)?
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digoxin blocks NaK ATPase in crdiac myocytes which lessens Na gradient --> less Na goes back into cell --> less Ca pumped out of cell (less NaCa exchanger activity -->More intracellular Ca -->increased contractility at the sarcomeres
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What drugs have each of the following side effects?
Agranulocytosis Osteoporosis Pulmonary fibrosis Gynecomastia Photosensitivity Drug-induced lupus |
clozapine, carbamazepine, colchicine, propylthiouracil, methimazole
corticosteroids, heparin (long-term) bleomyclin, busulfan, amiodarone spironolactone, amiodarone, tetracyclines sulfonamides, amiodarone, tetracyclines sulfonamides, hydralazine, isoniazid, procainamide, phenytoin |
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What adult structures are derived from 3rd, 4th, and 6th aortic arches?
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3rd--common carotid, proximal internal carotid
4th - left-arch of aorta, right+proximal part of right subclavian 6th - prox. part of pulmonary arteries, ductus arterioles |
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What agents stimulate the release of NE from the presynaptic button?
What agents potentiate the action of NE by inhibiting its reuptake into the presynaptic cell from the synaptic cleft? |
Amphetamine, ephedrine, and tyramine stimulate release
Cocaine and TCAs potentiate action by inhibiting its reuptake |
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Illustrate the Starling forces affecting capillaries.
Factors causing INCREASED Pc (capillary hydrostatic pressure) or pushing of fluid out of capillary causing EDEMA |
CHF (d/t incr central venous pressure
Venous thrombosis compression of veins (by tumor, cast, etc) sodium and water retention *increased capillary permeability will cause EDEMA and can come from infections and septic shock, toxins or burns *Decreased plasma colloid osmotic pressure (force pulling fluid into capillaries) can also result in EDEMA and can come from nephrotic syndrome, liver disease, protein malnutrition, protein-losing enteropathy *Increased interstitial colloid osmotic pressure (force pulling fluid into interstitial) can cause edema and can come from lymphatic obstruction |
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How do SVR and CO change in the following types of shock?
1.Hypovolemic 2.Cardiogenic 3.Sepsis /anaphylaxis 4. Neurogenic |
1following trauma/massive blood loss, low out put HF --cool skin; SVR:increase (raise BP), CO: decrease, Rx: IV fluids/blood
2heart isn't pumping from MI or PE, low output HF --cool skin; SVR: Increase (raise BP), CO: decrease, Rx: Dobutamine (ionotropic drug) 3. Cause vasodialation, high HF --hot skin, SVR: decrease; CO: increase (compensatory), Rx: Antiobiotics to treat infection IV fluids, NE (as a vasopressor if needed) 4.from brain or spinal cord injury, SVR: decrease, CO: decrease, Rx: IV fluids spinal cord injury + steroids |
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Locations of central lines:
* |
goes straight into major vein
*Femoral: easiest site, least risk, only stay in 5-7 days due to rise of infection *Subclavian (SC) easy to find, can remain 3 - 4 wks, not as uncomfortable; however highest risk of pneumothorax. not good choice for COPD or lung tumor *Internal jugular (IJ): good landmarks, can remain 3 - 4 wks, but more uncomfortable for pt., risk of puncturing the carotid or causing pneumothorax. Do not place left IJ without discussing it with staff, due to a greater risk of perforating the left SC vein due to the angle at which the left IJ and left SC meet.: Swan-Ganz catheter preferred sites: right IJ > left SC > right SC > left IJ |
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How do the following circumstances impact the Starling forces of fluid moving through capillaries?
1Heart failure: 2Liver failure: 3Oliguric renal failure: 4Infections and toxins: 5Nephrotic syndrome: 6Lymphatic blockage: 7Burns: 8Diuretic administration: 9IV inclusion of albumin or clotting factors: 10Venous insufficiency: |
.1. Increased PC, capillary hydrostatic pressure
2. decreased plasma colloid osmotic pressure (fluid will stay in interstitial due to lower proteins in blood 3. Incr. interstitial colloid osmotic pressure/ d/t incr proteins in interstitum (non-pitting edema) 4. increased capillary permeability, Kf 5. decr plasma colloid osmotic pressure (slued will stay in interstitial due to lower proteins in blood) 6. Incr interstitial colloid osmotic pressure d/t incr proteins in interstitium(non-pitting edema) 7. increased capillary permeability, KF 8. decr Pc, capillary hydrostatic pressure so less fluid forced into interstate\ 9. increase plasma colloid osmotic pressure 10. incr capillary hydrostatic pressure -->edema |
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How does the vascular resistance and stroke volume differ in hypovolemic shock compared to septic shock?
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Hypovolemic: Vascular resistance: up, SV down
septic shock: Vascular resistance: down (dilation), SV up |
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What are some of the causes of cardiogenic shock?
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MI, PE, CHF, Arrhythmias, cardiac tamponade, tension pneumo, cardiac contusion
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How is the skin of a patient different in cardiogenic shock compared to septic shock?
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cardiogenic shock pt would have cool, clammy cyanotic, poorly perfused skin
septic shock: warm and flushed skin because of vasodiltation |
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To what drug category does each of the following drugs belong?
1. 6-mercaptopurine 2. celecoxib 3.carmustine 4. doxycycline 5. Timolol 6. Methotrexate 7. Cimetidine 8 Mefloquine |
1anticancer
2. cox 2 inhibitor 3. nitrosurea 4. tetracyclines 5. beta blocker 6. dihydrofolate reductase inhibitor 7. H2 blocker 8. antimalarial |
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In the dark, both pupils are dieted, but in the light the control pupil is mitotic while the pupil given drug X remains mydriatic. What is drug X?
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sympathetic agonist (like epinephrine) or an anticholingergic (like atropine)
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What is the antidote for each of the following toxins?
1. Copper, gold, mercury 2. arsenic, mercury, gold 3. t-PA, 4. Digitalis |
1. penicillamine
2. dimercaprol, succimer 3. aminocaproic acid 4. anti-digoxin antibody fragments |
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4. When does isovolumetric contraction takes place?
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between closure of mitral valve and opening of aortic valve during QRS
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How does an increase in after load affect the stroke volume of the heart assuming contractility remains the same?
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decreases it
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What impact does an increase in contractility have on stroke volume assuming preload and after load remain constant?
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increase
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What heart sound is associated with dilated congestive heart failure? What heart sound is associated with chronic hypertension?
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S3 --dilated
S4 -- Chronic htn causing hypertrophy of LV |
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What gives rise tot he jugular venous a, c, and v waves?
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a - atrial contraction
c - ventricular contraction v -- atrial filling against closed tricuspid valve |
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Where does the QRS complex fall in relation to valvular dynamics?
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QRS = closure of mitral and tricuspid valves (atrioventricular valves)
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To what drug category does each of the following drugs belong?
1.Azathioprine 2. probenecid 3. primaquine 4. cefprozil 5. lamivudine 6. tobramycin 7. losartan |
1. immunosuppressive
2. gout 3. antimalarial 4.2nd gen ceph 5. NRTI 6. aminoglycoside 7.ARBs 8. HIV protease inhibitor |
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How does hemicholinium inhibit the transport of choline into the nerve terminal?
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inhibits Na co-transporter bringng Na and choline into cell
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Which brachial arches develop into the following structures?
1. common carotid artery 2. aortic arch 3. right subclavian 4. pulmonary arteries |
1. 3rd
2.4th on left 3. 4th on right 4. 6th |
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What heart sounds are considered benign when there is no evidence of disease?
1. Split S1 2. Split S2 on inspiration 3. S3 in a pt older than 40 yo 4. early quiet systolic murmur |
1. Split S1
2. Split S2 on inspiration 3. S3 in a pt older than 40 yo 4. early quiet systolic murmur |
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Which heart valves should blood be flowing through during systole? During Diastole?
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systole -- blood flows through aortic and pulmonic valves
Diastole -- blood flows through mitral and tricuspid valves |
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What are the diastolic murmurs?
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mitral/tricuspid stenosis
aortic/pulmonic regurge |
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What murmurs are heard best in the left lateral decubitus position?
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Mitral regurge, mitral stenosis, left-sided S3 and left-sided S4
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Bounding pulses, head-bobbing, diastolic murmur
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Aortic regurge
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Outline the pathway of converting phenylalanine to epinephrine
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phenylalanine --(phenylalanine hydroxylase) -->tyrosine -- (tyrosine hydroxylase) -->dopa -- (dopamine decarboxylase and B6) --> dopamine -->NE --> Epi
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Name 8 different indirect cholinergic agonists and state use for each.
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1. neostigmine -- neurogenic ileus, postop reversal of NMJ, tx of Myesthenia Gravis
2. pyridostigmine -- tx of myasthenia gravis 3. Edrophonium -- Dx of MG 4. Physostigmine -- atropine overdose 5. Echothiophate -- tx of glaucoma 6. Alzheimer drugs -- Donepezil, galatamine, rivastigmine |
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Outline the flow of fetal circulation.
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1, umbilical vein --> ductus venosus (mixing of blood in liver) -->IVC --> right atrium -->foramen oval --> left ventricle -->aorta-->system circulation-->umbilical arteries-->placenta
2. umbilical vein-->ductus venosus (mixing of blood in liver)-->IVC-->right atrium-->right ventricle-->left atrium-->foramen oval-->right atrium?? 3.umbilical vein-->ductus venosus (mixing of blood in liver)-->IVC--> right atrium-->right ventricle arterioles-->aorta-->system circulation-->umbilical arteries-->placenta |
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What are the most common causes of aortic valvular stenosis?
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Bicuspid aortic valve
Senile (degenerative) calcification Rheumatic valve disease Congenital unicuspid aortic valve Syphilis |
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Which heart murmur is associated with weak pulses?
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aortic stenosis
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Which pathology is assoc. with each of the following murmurs?
1. Crescendo-decrescendo systolic murmur best heard in the 2nd -3rd right interspace close to the sternum 2. Early diastolic decrescendo murmur heard best along the upper left side of the sternum 3, Late diastolic decrescendo murmur heard best along the lower left side of the sternum 4 Pansystolic (AKA holosystolic) murmur best heard at the apex and often radiates to the left axilla 5.Late systolic murmur usually preceded by a mid-systolic click 6. Crescendo-decrescendo systolic murmur best heard in the 2nd-3rd left interspaces close to the sternum 7. Pansystolic (AKA holosystolic) murmur best heard along the left lower sternal border and generally radiates to the right lower sternal border 8. Rumbling late diastolic murmur with an opening snap, heard loudest in the 5th interspace in the midaxillary line 9. Continuous machine-like murmur (in systole and diastole) 10. High-pitch diast.mur with widened pulse pressur |
1.aortic stenosis
2. pulmonic regurge 3. Tricuspid stenosis 4. Mirtal regurge 5. Mitral valve prolapse 6.Pulmonic Stenosis 7. VSD or tricuspid regurge 8. Mitral stenosis 9. PDA 10. aortic regurge |
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A gardener presents with shortness of breath, salivation, mitosis, and diarrhea. What caused this? What is the mechanism of action?
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organophosphate poisoning
inhibition of acetylcholinesterase-->excess cholinergic stimulation of muscarinic receptors |
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What is the mechanism of action of N-acetylcysteine when given as an antidote for acetaminophen overdose?
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regenerated glutathione
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What is the equation for half-life?
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t 1/2 = (0.7 Vd)/CL
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Diagram the phases of myocardial action potential and
describe which ion channels are responsible for each phase. |
Phase 0 = Na channel open --> rapid depolarization
Phase 1 = Na channels open a little and K channels begin to open-->early depolarization Phase 2 = voltage gated Ca channels open to balance out K channels-->plateau (cause more Ca release to cause myocyte contraction) Phase 3 = Massive K influx and Ca channel closure --> depolarization Phase 4 = resting membrane potential due to K channel permeability |
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Describe the flow of ions during a pacemaker action potential
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Phase 4 = slow increase in sodium conductance-->depolarization to threshold
Phase 0 = Ca channel opening -->conduction Phase 3 = inactivation of Ca channels and increased activation of K channels-->depolarization |
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What physiology accounts for the automaticity of the AV and SA nodes?
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Phase 4 gradual sodium conductance in phase 4 of pacemaker action potential
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What are the 4 most important pharmacokinetic equations?
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CL = 0.7Vd/half-life
MD = Css x CL LD = Css x Vd Vd = D/c = amt of drug given IV/Concentration of drug in plasma |
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What G protein class does each of the following receptors simulate?
1) a1 2) a2 3) B1 4)B2 5)M1 6) M2 7) M3 8)D2 |
1) q 2) i 3) s 4) s 5)q 6)i
7) q 8) i |
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What enzyme is inhibited by the drug fomepizole?
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alcohol dehydrogenase
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1. Class iA 2. Class 1B 3. Class IC (all phase 0)
4. Class II ( phase 4) 5.Class III (phase 3) 6. Class IV (phase )) |
1. Quindine, procainamide, disopyramide
2. lidocaine, mexilente, tocainide 3. flecainide, propafenone 4. metaprodol, proprandol 5. sotdol, amiobrone,ibutilide, dofetilide 6. diltiazem, verapamil |
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What is the mechanism of action of each class of anti arrhythmic?
Class I Class II Class III Class IV |
Class 1 = Na channel blockers
Class II = B-blockers Class III = K channel blockers Class IV = ca channel blockers |
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Which anti arrhythmic has the side effect of cinchonism?
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Quinidine
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What are the potential side effects of amiodarone use?
|
pulmonary fibrosis, hyper/hypothyroidism, hepatotoxicity are the big ones
also: blue-grey skin, photodermatitis/photosensitivity, bradycardia, heart block, corneal deposits, neuro problems, constipation |
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What is the mechanism of action of adenosine as an anti arrhythmic?
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Increases outward K current causing hyper polarization of cells
decreases intracellular calcium |
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To which class of antiarrhythmics does each of the following agents belong?
1. sotalol 2. propranolol 3. bretylium 4. quinidine 5. verapamil 6. procainamide 7. lidocaine 8. diltiazem |
1. III 2. II 3. III 4. IA 5. IV 6. IA 7. IB 8. IV
|
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To what class of medication does each of the following drugs belong?
1. Primaquine 2. Saquinavir 3. Betaxolol 4. Prozosin 5. Thiopental barbiturate 6. Tranylcypromine 7. Sertaline 8. Temazapam 9. Desipramine 10. Captopril 11. Busulfan 12. Moxifloxacin 13. Zanamir 14. Miconazole |
1. antimalarial 2. HIV protease drug 3. B1-blocker 4. alpha-1-antagonist 5. barbiturate 6. MAOI 7. SSRI 8. benzodiazepine 9. TCA 10. ACE 11. DNA alkylating agent (anti-cancer) 12. flouroquinolone 13. anti-viral 14. antifungal
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What effect will a noncompetitive antagonist have on
V max and Km? |
Non-competitive -- decrease Vmax; Km stays same
|
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What pathology is associated with each of the following murmurs? 1. Crescendo-decrescendo systolic murmur best heard in the 2nd-3rd right interspace close to the sternum. 2. Rumbling late diastolic murmur with an opening snap 3. Pansystolic (AKA holosystolic or uniform) murmur best heard at the 4th-6th left intercostal spaces, adjacent to the sternum. 4. Continuous machine-like murmur (in systole & diastole)
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1. aortic stenosis
2. mitral stenosis 3. tricuspid regurge or VSD 4. PDA |
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The Six Limb Leads
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Unipolar limb leads (diagram)
Bipolar limb leads (diagram) |
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(chart) ECG Axis
Common conditions that result in axis deviation: Left axis deviation: (5 things) Right axis deviation: (5 things) |
Left axis deviation: inferior wall myocardial infarction, left anterior fascicular block, left ventricular hypertrophy (sometimes), LBBB, High diaphragm
Right: Right ventricular hypertrophy, Acute right heart strain (ex. massive plum. embolism), left posterior fascicular block, RBBB, Destrocardia |
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How does the cause of a narrow QRS compile differ from the cause of a wide QRS complex?
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Narrow QRS -- beat conducted through normal conduction pathway (through AV node and down perkinje)
Wide QRS -- Premature Ventricular contraction (PVC), Ventricular tachycardia, bundle branch block |
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What is the ECG axis given the QRS deflections in each of the following scenarios? 1. positive in lead I, positive in lead II 2.positive in lead I, negative in lead III 3. Negative in lead I, positive in lead III 4. Positive in lead I, negative in aVR
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1. normal axis
2. left axis deviation, or normal 3. right axis deviation 4. normal axis |
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How does hyperkalemia affect the shape of T waves?
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tall peaked t wave
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What is the vasopressor of choice for anaphylactic shock? Cardiogenic shock? Septic shock?
|
Epinephrine ---anaphylatic
Dobutamine -- cardiogenic NE ---septic |
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On auscultation of a patient, you hear a pan systolic murmur at the apex with radiation to the axilla. What is the most likely cause of this murmur?
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Mirtal regurge
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What drug inhibits the cellular sodium-potassium ATPase?
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Digoxin
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Drugs that prolong the QT interval ( 5)
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1. Anti-infectives: macrolides, chloroquine
2. Anti-psychotics: haloperidol, risperidone 3. methadone 4. anti-HIV protease inhibitors (-navirs) 5. antiarrhythmics: class IA (quinine) and class II (K= channel blockers such as stall) |
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What is the initial treatment for ventricular fibrillation?
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CPR and Defib
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What is the initial treatment for ventricular tachycardia when there is no pulse?
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CPR and Defib
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What is the hallmark of a third degree heart block?
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no connection btw atrial (P waves) and ventricular rhythm (QRS)
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What drugs are known to prolong the QT interval, increasing the likelihood of torsades in those at risk?
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Macrolides (erythromycin), anti-malarials(Chloroquine), HIV protease inhibitors (-navir),Clas IA, III antiarrythmics, Anti-phychotics (haloperidol, risperidone)
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What are the two different types of second degree AV block? How do they differ?
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Mobilz Type I (wenckebach)---progressively prolonged PR interval before a dropped beat
Mobitz Type II -- dropped beat with no warning |
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Why is warfarin anticoagulation important in patients with chronic atrial fibrillation?
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atrial stasis can lead to coagulation with thrombus --> embolism
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