Cardio/Hemo Flashcards
What artery feeds the Papillary Muscles?
What feeds the Interverntricular Septum? Blockage can lead to?
RCA
LAD: heart block (2 mobitz or type 3)
Type of Collagen Present in MI Scar? Risk of? Leading to?
Type 1, Aneurisym=Mural Thrombus
What occurs within 1 day of MI? Greatest risk of?
If Reperfused?
Coagulative necrosis (loss of cell nuclei). Arrthymias.
Contraction band necrosis (from return of Ca); and Reperfusion injury (from increased O2 generating free radicals; raising cardic enzymes Troponin I and CKMB)
What occurs within 1 wk of MI? Greatest risk of?
Yellow pallor:
Days 1-3 Neutrophils infiltration. Greatest risk for fibrinous pericariditis (if transmural infarct)******
Days 4-7 Macrophages come in and debride area. Greatest risk for rupture. A) Wall=Cardiac Tamponade. B) Septum=Shunting of blood C) Papillary Muscle=Mitral Insufificieny (Paps fed by RCA)
What occurs within 1 month of MI? Greatest risk of?
Granulation tissue to Scar formation (Type 1 collagen). Increased risk of aneurisym leading to mural thrombous formation.
Truncus Arteriosus, Tetralogy of Fallot
22q11
ASD > VSD, AV Septal Defect (endocardial cushion defect)
Down Syndrome
Biscupid Aorta Valve, Coarcation of the aorta (preductal)
Turners
MVP, thoracic aortic aneurysm and dissection, aortic regurg
Marfan’s
Tranposition of the Great Vessels
Maternal Diabetes
22q11
Truncus Arteriosus, Tetralogy of Fallot
Down Syndrome
ASD > VSD, AV Septal Defect (endocardial cushion defect)
Turners
Biscupid Aorta Valve, Coarcation of the aorta (preductal)
Marfan’s
MVP, thoracic aortic aneurysm and dissection, aortic regurg
Maternal Diabetes
Tranposition of the Great Vessels, Fetal Macrosomia, Caudal regression syndrome, hypoglycemia, hypocalcemia, and hypertrophic cardiomyopathy
Congenital Rubella
PDA, septal defects, pulm A stenosis
PDA, septal defects, pulm A stenosis
Congenital Rubella
Tuberous Sclerosis
Cardiac Rhabdomyomas, Renal Cysts, mental retardation, angiofibromas
What is Microangiopathic Hemolytic Anemia? Name and describe two conditions in which this occurs?
Small thrombi form in microvessles causing schistocytes. The thrombi formation causes thromboycytopenia.
HUS: Ecoli O157H7 endothelial toxin (shigalike toxin/ecoli verotoxin) exposing subenothelial collagen particularly occuring in renals.
TTP: def of ADAMSTS13–cannot cleave vWF multimer, thus getting microthrombi.
vWF is made in the weibel palade bodies of endothelial cells (WP bodes: W for vWf and P for P-selectins used in leukocyte extravasation.
Targets of Antiarrhythmics drugs?
Class I and III target ventricles
Class II and IV target AV node
1=Na, 2=Beta blockers, 3=K blockers, 4=Calcium blockers
“No Bad Boy Keeps Clean”
Symptoms of TTP/HUS
TTP vs HUS?
Labs of both?
“CRAFT”
Cns, Renals, Anemia, Fever, Thrombocytopenia
TTP(MOSTLY CNS)
HUS=mostly renals (uremia!)
Labs: Prolonged bleed time (thrombocytopenia), NORMAL pt/ptt time (adhesion of platelts but not activation thus no PT/PTT changes), hemolytic anemia
What are the granules of Endothelial Cells called and what do they contain?
Weibel Palati (sp?) bodies:
W for vWF
P for P selectin
What are the presentations of platelet disorders vs clotting factor disorders?
Platelet: Superficial bleeding (particularly Nosebleeds). Elevated clotting time.
Clotting Factors: Deep bleeds in tissues, joints, organs. Or Rebleeding after surgery. Normal Clotting time, slow PT and/or PTT.
CD Markers for:
1) HSCs
1) CD 34+
TTP vs HUS.
Causes, Mechanisms, Labs and Sxs.
TTP:
a) x ADAMSTS13 either congentially or usually autoimmune. b) Causing inabilty to cleave vWF penatmers, leading to microthrombic hemolytic anemia. c) Labs: Prolonged bleeding time with normal PT/PTT (just consuming platelets not factors (no activation of platelets. D) “CRAFT”: CNS, Renal, Anemia (schistocytes), Thrombocytopenia.
HUS:
Ecoli 0157H7 (EAEC). Usually from eating undercooked meat. Hemolytic anemia from Shiga-like toxin damaging endothelial cells (particularly in renals) causing exposure of subendothelial collagen leading to microthrombi. MORE RENAL INVOLVMENT. Don’t give antibiotics because you kill the normal gut flora first alleviating EAEC’s gut competition.
ITP
Mechanism, presentation, labs
Immune Thrombocytopenic Purpura. Antibodies (IgG) to platelets. Longer bleed time with normal PT/PTT. Usually present in a middle aged female.
Bernard Soulier
Def in Gp1b. Stopping Platelet adhesion and thrombocytopenia.
“BS” big suckers from immature platelets.
“Soiler ~ soil platelets cannot adhere to soil”
Glanzmann Thrombocytopenia
Broken Gp2b/3a (abciximab does the same thing). Impairment of platelet aggreation.
Throbmo (platelet) sthenia (weak) = weak clot.
Hemophilia A: Presentation, mechanism
Hemo B (Christmas’s disease)
Coagulation factor inhibitor mixing study?
F8 def (“AAEIGHT”).
Common sporadic mutation, Deep tissue joints and surgical rebleeds.
X-linked (boys!). Normal bleed time, normal PT and prolonged PTT
F9 def, rarer.
Autoimmune targeting of F8 or 9. Presents similiarly as Hemo A/B. Mixing study will NOT show clotting.
vWF deficiency
Mucuosal and Skin bleeding (from poor platelet adhesion)
Most common INHERITIED def.
vWF stabilizes F8 (def of that too)
Labs: delayed clotting time, with prolonged PTT (but don’t see deep bleeds phenotype, just on labs)
Liver Failure causes what factor defs?
Monitor liver failure with?
Deficiencies in 2, 7, 9, 10, C, S.
Monitor via the PT*** (cuz that whole pathway is produced by the liver, and makes sense since this is also what you use to monitor Heparin (which inhibits epoxside targeting of liver produced factors)).
HIT
Heparin Induced Thrombocytopenia.
IgG against Hep-Platelet F4 complex
Spleen removes IgG bound platelets.
Tx: Stop heparin and give a direct thrombin inhibitor.
DIC
Consumption of platelets and factors (prolonged bleed, PT, PTT).
Causes: Amniotic fluid (high in tissue factor), sepsis (LPS–>IL-1+TNFa), Mucin (from adenocarcinoma), PML (MPO in Auer Rods), Rattle Snakes.
Microthrombitic Hemolytic Anemia.
Elevated D-Dimers (F13 crosslinks, very sensitive, not speicific)
Aminocaproic Acid?
Inhibits activiation of Plasminogen (thus a “procoagulant”)
Plasmin Overactivity Or def of Alpha 2 antiplasmin resembles___?
But you differentiate it with___.
Resembles DIC too much chewing up of clot AND prevention of clot formation (plasmin cleaves fibrin, fibrinogen, and inhibits platelet aggregation)
Thus resembles DIC however on labs you will see NO D-DIMERS cuz clots never have a chance to form.
Protein C or S def?
What does it put you at risk for?
Normally degrade the other two with cofactors (8 w/ 9 and 10 w/ 5), so a def is a procoagulable state.
This puts you at risk for Warfarin induced skin necrosis*****
Factor 5 Leiden
Mutation rendering F5 uncleavable by Protein CS
Most common hypercoagulable state.
Prothrombin 20120A, type of mutation?
Increased gene expression of prothrombin thus hypercoag
AT3 Deficiency
AT3 is what cleaves thrombin and it is what Heparin binds to.
These patients will not respond to heparin (won’t see the increase in PTT, until VERY high doses).
What do OCPs do to the cascade?
Estrogen induces the increased production of coagulation factors thus promoting a procoagulable state.
Labs for Anemia of Chronic DIsease vs Iron Def anemia
(also what’s the supposed mechanism of ACD?)
Il-6 causes release of acute phase reactants including Hepciden, which inhibits EPO and causes ferroportin internalization from basal membrane of enterocytes (and macros) thus preventing release of iron into blood.
Iron Def: Microcytic, decreased iron, ferritin, and % saturation with INCREASED TIBC,
ACD: Microcytic, HIGH FERRITIN, LOW TIBC, low iron (taken up by marrow just not replenished).
- Location of Hb synth during devo
- HbH
- HbBarts
- # of genes in alpha thal
- what’s seen in severe alpha thal
- # of genes in beta thal
- whats seen in severe beta thal
- Risk for in beta thal*****
- Young Liver Synthesizes Blood (Yolk, Liver, Spleen, Bone)
- beta tetramer
- gamma tetramer (associated with hydrops fetalis)
- 4 genes on Chromo 16
- Hydrops fetalis; trans mutation in asians (might be why there’s a higher rate of spontaneous abortion
- 2 genes on Chromo 11
- Codocytes (alpha aggregates) can cause extravascular hemolysis, massive erthroid hyperplasia (spleenomegaly and skull/chipmunk facies);
- risk for aplastic anemia with Parvo B19 (non-enveloped SS linear DNA = “Parvo NESSLD in HSC”)
Clinical Features of
Extravascular Hemolysis vs Intravascular Hemolysis
Extra: ANEMIA WITH SPLENOMEGALY, Jaundice dt unconj bili, increased risk for cholelithiasis
Intra: Decrease Haptoglobin Levels. Hemoglobinemia, hemoglobinuira, hemosiderinuria (epithelial cells of Renal Tubules absorb iron and slough off several days later).
Hereditary Spherocytosis
Def in Ankrin, Spectrin or Band 3.1.
Membrane bleds off as it passes thru reticulin gates of splenic reticuloendothelial system.
Increased RDW, increased MCHC (mean corpuscular Hb concntation=loosing membrane without losing Hb), Howell Jolly Bodies.
SPlenomegaly, jaundice, gallstones, increased risk for aplastic crisis from Parvovirus B19 (“NESSLD in HSCs”).
WORK HYPERTROPHY OF SPLEEN. Dx with Osmotic Fragility test.
HbC
Auto Recessive, Glut–>Lysine
“C, crystals, lySIne”
Sickle
Increased Risk for Aplastic anemia (dt B19, NESSLD in HSCs), Osteomyleitis from Salmonella, Extravascular (w/ some intravascular)
PNH
Loss of DAF (CD55) and MIRL (membrane inhibitor of reactive lysis) thus cannot inhibit C3 convertase.
Due to ACQUIRE loss of GPI******
Fragments of platelets cause thrombosis (cause of death)***
G6PD def
Inheritance pattern?
Heinz Bodies (precipated Hb from oxidative stress), Heinz bodies removed resulting in BITE cells.
Intravascualr hemolysis
2) X-linked recessive—cuz the cells get x’ed (killed)
Immune Hemolytic Anemia
Warm vs Cold agglutinins associated with SLE or other autoimmunes.
Warm (SLE, Methyldopa, Hydralazine, Penicillin as hapten)
Cold (IgM, previous Mycoplasma pneumonaie and infectious mononucleosis)
Anticoagulants
pg 376 on first aid
Aspirin
Prophylactic Anticoagulant via cox inhibition Cox1 necessary for arachoidonic acid to Thromboxane (TxA2) conversion which causes platelet degranuation activating other platelets
Celecoxib
Antiinflamm Cox 2 inhibitor
Clopidogrel
Plavix, Antiplatelet, interferes with ADP receptor on platelets preventing their activation (and expression of GPiib/iiia)
Eptifibatide
Antiplatelet drug made from pit viper venom Potent GP2b/3a inhibitor (thus stopping fibrinogen from binding) Used in procedures
Tirofiban
Similar to Eptifabatide
Warfarin
Anticoagulant–Vit K Epoxide Reductase inhibitor Inhibits the production of the coagulants 2, 7, 9, 10 and the anticoagulants Protein C and S. All factors need GLA residue and are synthesized in the liver (remember if it needs GLA = made in liver) Tests extrinsic pathway: “Go to WAR with your Exs” C and S have shorter half lives; F2 (thrombin) has the longest half life (4 days)—therefore for the first 4 days pnt is actually in a prothrombotic state
abciximab
ReoPro, Prevents platelet acivation (thus anti-aggregation), anti-integrin monoclonal antibody binding Gp IIb/IIIa Think “ab in name inhibiting IIb/IIIa”
Tissue Plasminogen Activator (tPA) Alteplase
Antithrombolytic, Converts Plasminogen to Plasmin which then goes and degrades fibrin clots Used for acute stroke therapy
Aminocaproic Acid
t-PA Antidote thus ProCoagulator In the fibrolinolytic inhibitors class
Bivalirudin
Direct Thrombin Inhibitor Short half life, used for PCIs (percutaneous coronary interventions) in patients with HIT (heparin induced thrombocytopenia)
Argotroban
Direct Thrombin Inhibitor Derivative of arginine, used to anticoagulation in patients with HIT
Protamine Sulfate
Heparin Antidote From Fish sperm
Heparin
Anticoagulant Allosterically Catalyzes (activating) Antithrombin 3–>which then can bind to and act as a suicide inhibitor for Thrombin (2a) and Factor 10a; Risk for HIT (Heparin Induced thrombocytopenia)–autoantibodies to F4 Heparin complex=paradoxically causing increased clots with low platelet counts (also see hyperkalemia dt aldosterone inhib, and Elevated aminotransferase lvls) HEP (3 letters) tests PTT (3 letters)–intrinsic pathway (2 ts in relationship)–thus 11, 9, 10, 2 Unfractionated (HMW)=more specific for thrombin Enoxaparin (Lovenox)–Low Molecular Weight Heparin more specific for 10a; this means less inhibition of platelet aggreation cuz F10a doesn’t interact with platelets;longer half live then HWM Fondaparinux (Arixtra)–Pentasaccaride Heparin (smallest) and longest half life, NO Heparin Induced Thrombocytopenia (HIT)
Dabigatran
Thrombin inhibitor Oral, not reversible but dialyzable, 2x/day
Rivaroxaban
Anticoagulant: F10a inhibitor Oral, Not reversible but dialyzable, 1x or 2x/day
Digitalis
Slows conduction at AV node, and STIMS Vagal nerve=decreased HR***
SES: CHANGES IN COLOR VISION, VTACH***, anorexia, nausea, vomitting, diarrhea HYPERKALEMIA*****
Cardiac Glycoside–1) Improves contractility of failing heart, 2) Prolongs Refractory Period at AV node (good for SVTs) Mechanisms 1) Inhibition of NA/K atpase which stops the cell from clearing Ca allowing for longer contractoin. 2) Slows conduction velocity and increases refractoriness: Increases PSNS, and decreasing SNS
Isoproterenol
Sympathomimetic: Heart stimulation in bradycardia or heart block
Dobutamine
Sympathetomimetic—Acute Heart Failure Increases Inotopy (slighty chrono) “dope up someone with heart failure”
Pheynylephrine
Vasoconstrictive effects used to treat hypotension, shock (alpha 1 agonist) Nasal decongestion (topical), ophthalmic effect (topical)-mydriasis
Anti-hypertensive Targets
Diruetics Direct-acing vasodilators alpha adrenergic blockers centrally active SNS inhibitors b adrenergic blockers clacium antagoinists ACE inhibitors (NOT WITH PREG) -opril ARB (angiotensin recptor blcokers) (NOT WITH PREG) -sartans Direct renin inhibitiors (NOT WITH PREG) aliskerin
Albuterol
Asthma, COPD for Bronchodilation B2 agonist
Clonidine (as opposed with Clozapine)
Antihypertensive (Alpha 2 agonist penetrating BBB), diminishes cravings in narcotic alcohol and nicotine withdrawal, Tx for ADHD Penetrates CNS—inhibits CNS output. Produces Hypotension, bradycardia, sedation (clozapine=atypical antipsychotic known to cause agranulocytosis and seizures)
Phenoxybenzamine
Pheochromocytoma Tx “Ph-uck specificity, PH-eochromocytoma” Nonspecific alpha adrenergic blocker
Beta-Blockers
“-olol”s best tx for angina*** Tx: Angina, HTN, SVTs, Vtachs, MIs, Hyperthyroidism, gluacoma, migraine, tremor, Heart failure
SEs: MASK THE EFFECTS OF HYPOGLYCEMIA, IMPOTENCE, EXACERBATION OF ASTHMA
Phentolamine
Tx for hypertensive crisis Short term Competitive Alpha blcoker “Ph-uck specificity, PH-eochromocytoma
Methyldopa
Anti-hypertensive used in pregnancy “m-eth and dope for soon to be mommys”
Diltiazem Verapamil Nifedipine
Antihypertensives: Calcium Channel Antagonists D and V - lower HR and inotropy, and nodal conduction; increase peripeheral vasodilation Nefidipine: major peripheral dilator, less heart effects
Hydralazine, MIdoxidil Nitroprusside
Direct Vasodilator, used for HTN crisis “Midoxidil DILATES”–rogaine Nitroprusside has a cyanide toxicity; monitor thiocyanate levels
Hydralazine, MIdoxidil Nitroprusside
Direct Vasodilator, used for HTN crisis Hyralazine–Drug Induced Lupus, used to Tx HTN in Pregnancy (same as methyldopa) “Midoxidil DILATES”–rogaine Nitroprusside has a cyanide toxicity; monitor thiocyanate levels
Colestipol Cholestyramine Colesevelam
Bile acid sequestrants Less bile acid absorbed (thus less fat absorbed) and more cholesterol used to replace bile Interferes with vitamin absorption
Statins
HMG-CoA reductase inhibitiors
TERATOGENIC,
myopathy, rhabomyalisis (esp with fibrates/niacin)
drug interactions “Preg women STAy away from STATINS”
Ezetimibe
Cholesterol Absorption Inhibitor Inhibts NPCL1 at brush border (transport protein in hepatocytes; neimann pick like C1)
Ez Diarrhea
Cholestyramine, colestipol, colesevlam
Bile acid binding resins (people hate the taste)
Cholestyramine binds C. Diff Toxin
Fibrates
PPAR alpha agonist
Increases LPL thus TG clearance, and induces HDL synth
Myositis (particularly with statins). Hepatotox (up LFTs),
Niacin (nicotinic acid, Vit B3)
Blocks production of VLDLs; “Niacin is a V-itamin blocking V-ldls”
HYPERGLYCEMIA AND HYPERURICEMIA (GOUT
Nifedipine
Calcium channel blocker: Vasodilator-can be used in High Altitude Pulm/Cereberal Edema (HAPE, HACE) to vasodilate and lower BP Dihydropyridine (DHP) Ca entry blocker Systemic vasodilation (arteries>veins; thus decreased afterload; nitrates do veins more), also vasodilates coronary arteries leading to better perfusion/O2
Antiarrhthymic Drugs
Class 1: Na channel blockers -1a: Prolongs action potential duration (procainamide) -1b: shortens action potential duration (lidocaine)–used to break arrhythmias -1c: Slows depolarization phase of AP without significantly affecting overall length Class 2: Beta blockers: decreasing SNS–>SVTs via decreased AV node conduction Class 3: Potassium blockers: Prolongs action potential duration (amiodarone, sotalol, ibutilide) Class 4: Cardiac calcium blockers (verapamil and diltiazem) Adenosine, magnesium, digitalis, digibind antibodies
Verapamil
Class 4 Antiarrhtymic and Vasodilator moderate vasodilation, modest decrease in CO and HR contraindicated in CHF (more suppressive Heart effects than Diltiazem)–“VeRAPamil get a bad rap in the heart”
Quinidine? SEs?
Type 1a antiarrthymic
Cinchonism: flushing, tinintus, headache, vision, vertigo, dizziness, nausea, vomitting, diarrhea
Diltiazem
Class 4 Antiarrhtymic and Vasodilator Diltiazem–“Dilates and ZEN’s the heart” moderate vasodilation, modest decrease in CO and HR less suppressive Heart effects than verapamil
Procainamide
Class 1a: slows up stroke of AP
USED FOR WPW*******
SEs: LUPUS ERTHEMATOSUS SYNDROME
Lidocaine
Class 1b antiarrhtymic: shortens AP by binding activated and inactivated Na channels Preferentially selects damaged cells (state dependent block—as they are omre likely to be depolarized); used to break ventricular arrthymias (tachys) and status epilepticus Amiodarone is being used more often now
Flecainide
Class IC antiarrthimic–SVTs (affects the His/Purkinje system preferentially) Blocks sodium channel (potent) CAN cause HF in patients with heart abnormalities, and increased mortiality in patients with MIs
Propanolol Esmolol
Beta blocker AV node is particularly sensitive, decreases the Phase 4 slope; also slows the slow pacemaker current thus slowing the pacemaker rate Esmolol: B1 selective blocker; SHORT half life (good for post surgery prevention of SVT), used to controll Ventricles in Afib/flutter –Also drug of choise for Aortic Dissection Contraindicated in WPW (but ok for other AVRTs)
Sotalol
Class III antiarrhythmics, Used for Ventricular arrhythmias and maintenance of sinus rhythm in patients with A Fib K+ blocker and Beta blocker; Reverse use dependent (affects less active cells more–higher risk of torsades) Prolong QT (repolarization)–increases risk of Early afterdepolarizations (which can cause torsades de pointes)
Amiodarone
Class III antiarrhythmics: Used for SVTs and VTs (Afib, fluttter, vtach, vflutter, SVTs w/ and w/o bypass tracts) Blocks Na, Ca, K and B adernergic receptors Not reverse use dependent–thus it blocks better at faster rates thus it: Rarely causes new arrhythmias but can Prolong QT (repolarization)–increases risk of Early afterdepolarizations (which can cause torsades de pointes) **PULM FIBROSIS RISK and GRAY MAN SYNDROME **New analogs: Dronedarone, vernakalant, ranolazine
Ibutilide and Dofetilide
Class III antiarrhythmics: Use for acute conversion of A fluttter and Afib Reverse use dependent (affects less active cells more–higher risk of torsades) Prolong QT (repolarization)–increases risk of Early afterdepolarizations (which can cause torsades de pointes)
Adenosine
Used for conversion of paroxysmal supraventricular tachycardia to sinus (SHORT HALF LIFE ~10secs) Activates K inward rectifier K current, inhibits Ca and If=Hyperpolarization and fewer APs
Magnesium
Antiarrhytmic effect (unknown mechanism) and tx for digitalis toxicity
Digoxin immune Fab
Used as adjunct for digitalis toxicity with magnesium Digoxin: inhbits Na/K atpase which then inhibits the Ca/Na exchanger (drug is used to increase inotrophy and control contractions)
Nitros
VENOdilators decreasing preload on the heart and thus myocardial o2 demand Increase GC activity which increase cGMP
SEs: HEADACHES (from vasodilation)
Sildenafil
Phosphodiesterase 5 inhibitor decreasing PDE5s break down of cGMP. VENOdilators used for erectile dysfunction. “-fils the Weiner. “
Aliskerin
Direct Renin inhibitor (similar effects to ARBs/ACEIs) Not for Pregnancy. “aliskerin scarrin’ renin away”
Dopamine
Used for acute CHF to increase inotropy; DA also increases vascular tone which is useful in HOTN
Dobutamine
Increasing HR during acute CHF withOUT increasing vascular resisitance B1-2 and Alpha agonist Used for increasing
Prazosin
Anti-Hypertensive, also used for BPH, and Urinary flow Selective Alpha-1 antagonist: -azosins Its a “sin” to uses azosins
Carvedolol
Beta blocker used in Chronic HF, used to prevent arrhtymias, prevent negative remodeling, and to prevent SNS hyperactivation. Other beta blockers stop the downregulation of B1 receptors in HF but carvedolol does not (thus it improves SNS resistance of the Heart)
What lipid drug combination is most likley to result in hepatotoxicity?
Statins (Simvastatin) and Fibrates (Gemfibrozil).
Fibrates increase the concentration of statins.
Bosentan
Tx for Pulm Arterial HTN (udt BMP2R which inhibits smooth muscle proliferation).
Mech: antagonizes endothelin-1 receptors which decreases pulm vascular resistance.
Digitalis Toxicity?
Fatigue, Changes in perception, color vision changes, nausea, vomitting, diarrhea, abdominal pain, headache, dizziness, confusion and delirium.
And HYPERkalemia
RENALY CLEARED
Aortic Arch Derivatitves?
Logically work your way down
1st: Maxilliary
2nd: stapedial/hyoid
3rd: Common and beginning of internal carotid***
4th: Aortic Arch (left), Right: Prox of R subclavian
6th: Ductus Arteriosus and Pulm arteries
CO = (2 forms?)
SV x HR
O2 consumption rate / Arteriovenous O2 difference (this is known as ficks principle)
Handgrip Maneuver does what to Heart sounds?
Increases Afterload:
Decrease ASten, and Hypertrophic Cardiomyo
Increase Mitral and Aortic Regurg and VSD
What does Valsalva do to heart murmurs?
(phase II): decrease preload (and afterload)
Increases: Hypertrophic Cardiomyopathy, Increases MVP and opening snap occurs EARLIER.
Decreases: Aortic stenosis, and most murmurs
MVP: decreased filling of LA causes there to be more regurgitant flow (louder) and an earlier opening snap******
Hypertrophic: Less volume in ventricle allows for more disruption of flow from hypertrophied septum in ventricle
Squatting effect on heart murmurs?
Increases Preload
Increases Aortic Stenosis
Decreases Hypertrophic cardiomyopathy, decreases MVP causing a late opening snap
MVP: increased filling of LA causes there to be less regurgitant flow and a later opening snap******
Hypertrophic: More volume in ventricle allows for less disruption of flow from hypertrophied septum in ventricle
Drugs that Prolong QT?
At risk for developing____ which can progress to _____?
“Some risky Meds can prolong QT”
Sotalol, Risperidone, Macrolides (Az prolongs the QT), Chloroquine, Protease inhibitors (navirs/previrs), Quinidine (Class 1a and III’s do it), Thiazides (increased Ca/dec K fucks up conduction)
Progressing to Torsades leading to Vfib
High BP sensing mechanism and circuit?
Carotids bodies—>CN9 (9 does parotids and carotids)
Aortic Body—>CN10
9+10–> Nuclues Solitarius (Vasomotor medullary center):
Stimulates CN10 (PSNS) onto Heart
Low BP sensing circuit?
ONLY Carotids not aortic bodies.
Carotids–>CN9–> Nuc Solitarious (Medullary Vasomotor):
1) This inhibits PSNS (less CN10 firing)
2) and Excites SNS–>Alpha 1 receptors–>inc bp
HTN, Bradycardia, and Respitory Depression (irregular breathing)?
Cushing Reaction:
Intracranial bleed causes ischemia which causes
ACE I SEs:
When don’t you use ACEIs/ARBs?
CATCCH
Cough (bradykinin)
Angioedema
Teratogenic
increase Creatinin
hOtn
hyperkalemia
(Rash)
Increased Renin
2) Renal Artery stenosis (risk decreasing perfusion to the point of ischemia)
AntiHTN that causes ototoxicity? especially with?
Loop diruetics w/ Aminoglycosides
Prinzmetal (variant angina): what is it?
Tx?
ECG findings?
Dx?***
Coronary artery vasospasm seen usually in younger ppl (triggers: Tobacco, cocaine, and triptins)
Tx: Nitros or Dihydropyrine (vascular: nifedipine) Calcium channel blockers. (DO NOT GIVE BETA BLOCKERS)
ST segement ELEVATION (other anginas: stable/unstable are ST depression)
DX: ERGONOVINE (stims alpha and 5-ht) used to dx Variant angina
Patient has pleuritic chest pain releived by leaning forward? Cause other findings?
Pericarditis. Friction rub, diffusely elevated ST segments with PR depression.
With long standing constrictive pericarditis you can get Kussmaul sign (increased JVD upon inspiration)
Patient has systolic hypotension, distended neck veins, and distant heart sounds? Their condition? Other findings including EKG?
Beck’s Triad of Cardiac Tamponade
Pulsus Paradoxus
Electrical Alternans (heart moving around in the pericaridal “fluid sack”)
Young adult with liver problems presents with GI pain, melena, HTN, cutaneous eruptions and renal damage? What is it? What’s it associated with?
Polyarteritis Nodosa.
Hep B positive
Patient presents with delayed rumbling diastolic murmur. What type? Associated with?
Mitral Stenosis associated with opening snap.
Early opening snap (closer to S2=worse prognosis; signifying increased LAP)
Lipid Lowering Drug?
Mech, SEs (especially with?)?
Statins, HMG CoA reductase inhibitors.
Monitor LFTs and risk for rhadbomyolysis (especially with Fibrates/Niacin)
HDL raising and VLDL lowering drug?
SEs?
B3 Niacin
Lower VLDL lowers LDL levels
Flushed face (tx aspirin), Hyperglycemia (acnathosis nigricans) and Hyperuricemia (exacebates gout)
Prevention of intestinal absorption of bile acids?
SEs?
Unique about drug?
BIle acid binding resins (eg colesevelam/colestipol)
Cholesterol Gall stones, Fat sol vit absorptoin issues.
INCREASE TGs***
Can bind C. Diff toxin
Cholesterol Absoprtion blocker?
Targets?
SEs?
Ezetimibe.
Neimann Pick like receptor.
Diarrhea, rare LFT increases.
Best Triglyceride lowering agent?
Mechanism (2)?
Best to prevent?
SEs?
Fibrates/Fibric Acid derivative (eg gemfibrozil)
1) PPARalpha causing inc LPL = increased TG clearance; 2) Inhibit 7alpha hydroxylase which makes bile from cholesterol (inc risk of stones)
Acute Pancreatitis (since its activated by inc TAGs)
Inc LFTs, Myositis (esp w/ statins), Cholesterol Gallstones (esp w/ bile resins)
Class 1 antiarrthymics?
Na blockers
“Double Quarter Pounder, Lettuce Tomatoes PIckles, Fries Please”
Disopyramide, Quinieidine Procainamide
Lidocaine
Flecaindie Propafenone
Hyperkalemia Tx?
Calcium gluconate to stabilize membrane
Insulin with glucose to get cells to uptake K (turns on Na/K atpase)
B2 agonist
Sodium bicarb (if acidotic)
Heparin:
binds to?
LMW vs High Molecular W?
Antithrombin 3
HMW (unfractionated) inhibits BOTH thrombin and F10
LMW inhibts ONLY F10
Given in HTN emergency?
Sublingually? (effects?)
IV? (effects?)
Nitroprusside: VENOdilates decreasing BP/preload
Fenoldopam: (DA derived benzo) arteriolar dialation, naturiuresis (INCREASES RENAL PERFUSION thus its even safe in renal comp pnts beyotch!)
PDE3 inhibitors?
Cilostazol, Dipyradimole
Increase cAMP in platelets preventing aggregation. Increase cAMP in endothelium causing vasodilation.
Ticlodipine?
SEs?
Antiplatelet Drugs: Block ADP Receptor preventing expression of GpIIb/IIIa
(like clopidigrel)
SEs: NEUTROPENIA (clopidgrel does NOT have this SEs)
Apolipoproteins:
E:
A-1
C-II
B-48
B-100
E: on E-verything but LDL (E-xtra remnant uptake)
A-1: “A-1 steak sauce on a CAT”: activates LCAT thus on chylo’s and HDL
C-II: LPL cofactor (Chylo’s VLDL, HDL)
B-48: Chylomicrons
B-100: binds LDL Receptor
Cause of Sudden Cardiac death?
SCD is death within an hour of event. Usually due to thromboembolism causing a fatal arrthmia–which is most often V Fib
Drug given during acute MI in COPD pnt? Which type and why?
Beta blocker, needs to be specific for B1.
Don’t want a non-specific beta blocker because it will block B2 causing bronchoconstriction***
Give metoprolol
Fibrates do what to cholesterol/bile?
Fibrates inhibit 7 alpha reductase which is used to take cholesterol to bile. Thus inhibition causes both and decrease in bile and increase in cholesterol causing increased chance for cholesterol gallstones
Major Proliferative stimuli for growth of atherosclerotic plaque comes from where?
Platelets.
Endothelial dysfunction causes platelet aggreation and activation releasing cytokines
Patient presents with fatigue, conjunctival pallor, and difficulty swallowing and spoon nails. Deficient in?
Iron Deficiency.
Plumer Vinson.
Antiarrthymic that shows QRS prolongation without prolonging the QT interval
Na channel blockers (1C)
Reticulocytes appear blue under Wright-Giemsa stain from?
Ribosomal RNA
Labs for Immune Thrombocytopenic Purpura?
Isolated Low Platelets, with possibly elevated monocyte %
Drug that can cause 2nd or 3rd degree heart block?
Verapamil (remember its gets a “bad rep”
When do you see the following cells?
Acanthocyte
Basophophilic Stippling
Bite Cell
Macro-ovalocyte
Ringed Sideroblast
Schistocyte
Spherocyte
Dacrocyte
Codocyte
Heinz Bodies
Howell-Jolly Bodies
Holy cow!
Acanthocyte: Cholesterol disregulation (abetalipoproteinemia)
Basophophilic Stippling: ACD, ETOH, Lead, Thal’s (“LATA basophillic stippling”)
Bite Cell: G6PD (sulfas, flouroquinolones, Antimalarials); won’t see in asplenia
Macro-ovalocyte: Folate, B12, Orotic Aciduria (no pyrimidines)
Ringed Sideroblast: Inc Iron dep in mitos: X-linked sideroblastic anemia, Lead, myelodysplaisa, AML, Vit B6 def (INH)
Schistocyte: DIC, TTP, HUS, Traumatic hemolysis (soldiers marching, mechanical heart valves)
Spherocyte: Hereditary spherocytosis: extravascular hemolysis as splenic macros remove membrane
Dacrocyte: “Tear cell”: Sick crying bone marrow–aplastic anemia and myelofibrosis
Codocyte: Target cell: HALT said the hunter: Hbc, Asplenia, Liver disease, Thal’s
Heinz Bodies: G6PD–denatured hemoglobin from excess oxidation
Howell-Jolly Bodies: ONLY IN ASPLENIC PATIENTS (or functional asplenia)–nuclear remanants not removed by splenic macros
Difference between nonhemolytic and hemolytic normocytic anemia?
Nonhemolytic will NOT have an elevated reticulocyte count (marrow issues)
Hemolytic will have elevated reticulocyte count (marrow compensating for destruction, can possibly have slighlty larger cells, cuz they are immature)
What type of Hb in Alpha thal? When/how does it present?
WHat type of Hb and cells in beta thal (major)? When/how does it present?
1) HbBarts (all gamma), HbH (all beta); In utero as hydrops fetalis (if severe enough)
2) HbA2 (alpha 2, delta 2); Marrow expansions (crew cut skull appearance, chipmunk facies, extramdullary hematoposesis=hepatsplenomeagly). Suseptible to Parvo b19.
X linked Sideroblastic anemia defect?
Other causes of nonheritdatyr sideroblastic anemia?
What is the sideroblastic portion and what is the basophilic stippling seen?
ALAS
Lead, ETOH***, b6 def (INH)
Lead poisoning: Sideroblast portions of cell are mitochondria with iron in them (since ferrochelatase is inhibited and in mito), and basophillic stippling portion is from lead inhibiting ribonuclease thus ribosomes build up in cell.
Aplastic Anemia
Myleofibrosis
Myelodysplastic syndrome
Myelophthisic anemia
Aplastic: Failure/destruction of myeloid SCs, usually dt offending agent/virus. PANCYTOPENIA with FATTY INFLITRATION (Dry bone tap). NO HSM
Myelofibrosis: HSM*** dt chronicity (think of Aplastic progressing to this). Atypical megakaryocyte activation results in fibroblast activation=fibrosis
Myelodysplastic=ineffective hemaotpoesis (DYSplastic NOT aplastic). Pancytopenia/or decrease in 1 cell type. Marrow shows disordered differentation
Myelophthisic Anemia; Space occupying lesion of bone marrow (mets associated with fibrosis)
Bleeding time, pT, pTT of thrombolytics? Why?
Suffix of thrombolytics?
Elevated pT/pTT with normal Bleeding time.
This is because they destory preformed fibrin/thrombin clots, deactivate activated coag cascade and prevent further activation of coag cascade
“-plase” alteplase/reteplase/tenecteplase
Aspirins effect on bleeding time, pt, ptt? Why?
Increases bleeding time, NO CHANGE in PT, PTT (affects platelet activation/aggregation by decreasing TXA2, and PGs but doesn’t touch clotting factors)
Aspirin’s effect on resp/met alk/acidosis?
Initial rapid respiratory alkalosis followed by “overwhelming” metabolic acidosis
Cilostazol/Dipyridamole MOA? Used for?
SEs?
PDE 3 Inhibitors causing
1) increased platelet cAMP = decreased platelet aggregation
2) Vasodilation
Good for intermittent claudication (and other vascular issues eg angina, stroke/TIA prevention etc)
SEs: Nausea, Headache, Facial Flushing, HOTN
Fat in Marrow vs Fibrosis?
Aplastic Anemia (Fat)
Fibrosis=myelofibrosis
Beta thal is a what type of mutation?
Premature Stop codon, causing a dysfunctional truncated protein
Lipofuscin is what? Result of what?
Wear and tear protein.
Result of lipid peroxidation.
Tx for hypertrophic cardiomyopathy? Why?
What should you not use?
Beta Blockers—decreases preload which allows for “widening” of LV allowing for decreased flow obstruction.
Avoid drugs that decrease preload (eg diruretics) and increase contractility (digitalis)
Echinocytes in?
Prickly cells seen in Pyruvate dehydrogenase deficiency
PK def makes PricKly cells***
Signal thought to initiate Atheroslcerosis?
PDGF recruiting Smooth muscle cells from tunic intima
Kernicterus in newborn has what effect on brain?
Increased unconj bilirubin unbound*** deposits in basal ganglia (cuz the blood brain barrier hasn’t fully formed there yet)
Perfusion to inferior surface of heart?
PDA from RCA
