One Lines Spring Exam 2

7/29/2019 One Lines Spring Exam 2

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Buzz word definition

Volume overload Series hypertophy

Presure overload Parallel hypertrophy

Labl excrescences as you age you develop filliform processes on mitral andaortic valve, probably from small thrombi

Brown atrophy Lipofuscin deposits in a small heart

Signs of aging More picardial fat, lambl e, lipofushin deposits, basophilicdegneration

Cardiovascular dysfunction Most common failure of the pump, obstruction to flow isatherscleoris, regurgitant flow is murmurs, shunter flow,

disorder of cardiac conduction, rupture of the heart or majorvessesl

Frank starling mechanism Increased filling volume dilates the heart and enhancescontractility

Contraction dysfunction Systolic dysfunction

Filling dysfunction Diastolic dysfunction

Pressure overloadhypertrophy

Concentric hypertrophy

Volume overload Ventricular hypertrophy

L heart failure Back up of blood in the lungs, poor peripheral perfusion,pulmonary edema, Kerley B lines, heart failure cells(hemosiderin laden macrophages), orthopnea, dyspnea,prerenal azotemia

Chf Always characterized by decreased CO and tissueperfusion

Most common cause of Rheart failure

Left heart failure

R heart failure Congestive hepatomegaly, centrilobular necrosis, cardiacsclerosis, cardiac cirrhosis, congestive splenomegaly,nutmeg livers, ascites, edema of the periphery


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75% blockage Stable angina

90% blockage Unstable angina

Apex, anterior wall of left

ventricle and ventricularseptum

LAD

Posterior of septum, base Right coronary or left circumflex

Lateral Circumflex

Dominant cause of IHD Insufficient coronary perfusion relative to demand

Prinzmetal angina Vasospasm

Unstable, crescendo angina Precipitated by progressively lower levels of physicalactivity preinfarction angina

MI Women more likely after menopause estrogen hascardioprotective effect

Most common MI Thrombosed coronary artery

Problems with MI Past 20-30 minutes you get cell death

4-12 hours Early coag necrosis

1-3 days Yellow tan infarct

10-14 days Collagen deposition

2 months Dense collagenous scar

Most MI Transmural

STEMI Transmural ST elevation

NSTEMI Subendocardial, non ST elevation

Triphenyltetrazolium chloridestain

MI shows up as pale zone, everything else is brick raid

Extension Infarcts may expand beyond their borders following the MI,repurfusion injury

Myocytolysis At periphery of infarct, vaculoar degeneration


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Contraction bands Eosinophilic intracellular stripes, layer of perfused vs deadtissue

Troponin Rises 2-4 hours, peaks at 48, stays elevated 7-10

CK-MB Rises within 2-4 hours, peaks at 24, stays elevated 72hours

Ruptures More common in free wall than septum, 3-7 days

Dressler syndrome Fibrinous pericarditis, following transmural MI

Mural thrombus Thrombus originates in the heart chamber

Chronic IHD Usually enlarged and heavy due to LV hypertrophy hearts

Sudden cardiac death Most common cause arrhythmia, Long QT or WPW

Systemic Left sidedhypertensive heart disease

Initially left ventricular hypertrophy then later itshypertension,

Pulmonary right sidedhypertensive heart disease(cor polmonale)

Most commonly after pulmonary embolism for acute,chronic results from R ventricular hypertrophy secondary tolung diseases

of all valve disease Stenosis of aortic and mitral valves

Mitral valve stenosis Rheumatic heart disease

Mitral insufficiency Mitral valve prolapse (myxomatuous degeneration)

Most common valve disease Calcific aortic stenosis, age related- wear and tear

Calcific aortic stenosis Heaped-up calcific masses within aortic cusps thatultimately protrude through the outflow into valsalva

Mitral valve prolapse Mid systolic click, key histologic change, myxomatousdegeneration, most common surgical repair or replacementof mitral valve


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Rheumatic fever Aschoff bodies, caterpillar cells, pancarditis, verrucae,MacCallum plaques, leaflet thickening, commissural fusionand shortening, and thickening and fusion of the tendinous

cords, MITRAL VALVE, STREP A, Jones criteria: migratorypolyarthritis, pancarditis, subcutaneous nodules, erythemamargination of the skin, sydenham chorea (neruo disorderwith rapid involuntary movements)

Infective endocarditis Hallmark is vegitations. Most common on previouslydamaged valves by strep viridans, S auerus most virulentIV drug users, prosthetic valve- epidermidis. Ringabcesses, emboli may be shed from vegitations leads toseptic infarcts, subacute endocarditis is less valvulardestruction, develop new fever and murmur is IE. Janeway

lesions nontender palms or soles, ossler nodes in pulp ofdigits, retinal hemorrhages roth spots

Liebman-sacks endocarditis Noninfected/ sterile vegitations in debilitated patientsassociated with systemic lupus

Carcinoid heart disease Episodic flushing of the skin, nausea, vomiting,TRICUSPID

Complications of artificialvalves

Thromboembolic complications, infective endocarditis,WARFARIN for life

Dialated cardiomyopathy Less than 40% EFImpaired contractilitySystolic dysfuncionAlcohol, preggos, sarcoiosisMural thrombiNaxos syndrome- disorder characterized by arrhymogenicRV cariomyopathy and hyperkeratosis of planar skinsurfaces that is associated with mutations in the geneencoding plakoglobin

Hypertrophic cardiomyopathy 50-80% EF

Impairment of complianceDiastolic dysfunctionHyptertensive heart disease , aortic stenosisBananna like configuration- bulgin of the ventricular septuminto the lumenMyofiber disarrayHarsh systolic ejection murmur


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Restrictive cardiomyopathy Decrease in compliance, resuling in impaired ventricularfilling during diastoleAmyloidosis

45-90% EF

Meckels diverticulum Rule of 2s failed involution of vitelline duct

Most common intestinaldevelopmental

Imperforate anus

Pyloric stenosis Congenital more common males, 2nd-3rd week of life andnew onset regurg nonbillious vomitting

Hirshbrung disease Congenital agonglionic megacolon, deficient migration ofneural crest cells, lacks both gut plexuses, RET mutations,

rectum always affected usually limited to rectum andsigmoid colon

Gastrochisis Membranous sac present

Zenker diverticulum Upper upper esophageal sphincter

Traction diverticulum Middle of esophagus

Epiphrenic diverticulum Lower of esophagus

Esophageal stenosis Most common from scarring from GERD

Esophageal webs Associated with GERD, normally upper esophagus anddysphagia

Plummer-Vinson akaPatterson Brown Kelly

Webs, glossitis, iron deficient anemia

Esophageal rings askaSchatzki rings

Similar to webs but circumferential and thicker

A rings Present at the distal esophagus

GERD Sqaumous to noncilliated columnar with goblet cells

Achalasia Increased tone of lower esophagus sphincter: incompleteLES relaxation, increased LES tone, and aperistalsis,primary=neurons, secondary= chagas


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Esophagitis Mallory-weiss= longitudinal lacerations with vomiting,Boorhave syndrome= distal esophageal rupture(catastrophic)

Candiadasis white grey pseudomembranes

GERD Hyperemia, more eosinophils, and basal zone hyperplasia.In preggos, obese, alcohol, hiatal hernia

Eosinophilic esophagitis High numbers of intraepithelial eosinophils, failure of highdose PPI and absence of acid reflux

Barret Esophagus Increased risk of andenocarcinoma, epithelial dysplasia isconsidered to be a pre-invasion lesion, presence of Gobletcells

Esophageal varices Rupture is a medical emergency, pt will have portalhypertension and cirrhosis

Adenocarcinoma Typically GERD, lower of esophagus, H pyloriassosciated with decreased risk of adenocarcinoma

Sqaumous cell carcinoma More in african americans, middle of esophagus, fromalcohol and tobacco; top is cervical, middle is mediastinalor partracheal, lower is gastric and celiac nodes

Acute gastritis NSAID, H pylori, surface epithelia is intact, presence ofneutrophils and active inflammation, erosion denotes theloss of the superficial epithelium, concurrent erosion andhemorrhage is termed acute erosive hemorrhagic gastritis

Acute gastric ulceration Round small, found anywhere

Most common cause ofchronic gastritis

Infection with H pylori

H pylori Associated with over crowding, predominantly antralgastritis, high acid production, virulence: flagella, urease,

adhesins, toxins. Multifocal atrophic glossitis, intraepithelialneutrophils and subepithelial plasma cells, lymphaggregates: MALT

Curling ulcer Severe burns

Stress Shock


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Cushing ulcer Increased intracranial pressure

Autoimmune gastritis Antibodies to parietal cells and intrinsic factor, usually in the

body, invasion of lymphocytes and macrophages,decreased acid production (achloyhydria), increasedgastrin, neuroendocrine hyperplasia


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BIOCHEMISTRY!!

BUZZ WORD DEFINITION

RLS of TCA Isocitrate to alpha ketoglutarate, isocitrate dehydrogenas

Energy generation in TCA NADH after isocitrate, alphaketoglutarate, and succinateGTP after Succinyl CoA, and FADH2 after succinate

Increases rate of TCA cycle ADP and calcium on RLS and increase calcium on alphaketoglutarate dehydrogenase

NADH inhibits Isocitrate dehydrogenase, alphaketoglutarate and malatedegydrogenas

Hydrolysis of thioester bond From acteyl coA, drives reaction forward

Alphaketoglutaratedehydrogenase Huge enzyme complex made up of 4 parts:E1: aplhaketoacid decarboxylase contains TPPE2: transcyclase containing lipoate, transfers acyl portionE3: dihydrolipoyl dehydrogenase, contains FAD

Decreased TPP From thiamine, leads to heart failure because alphakeotdyh. Doesnt work and heart relies on a lot of energy fromNADH

Sources of acetyl coA Beta-oxidation of fatty acids, from pyruvate via PDC, andseveral AA

1st step of ETC NADH CoQ oxidoreductase

2nd step of ETC Succinate dehydrogenase

3rd Step of ETC CoQ

4th Step of ETC Cytochromes Bc1 to oxidase

Oxidate phosphorylation Never reversible

Energy yield 2 ATP per NADH, 1.5 ATP for FADH2, major source of heat

MERRF Myoclonic epileptic ragged red fiber diease, mitochondriahave too many cristae, DNA mutations in Lysine tRNA

ATP synthesis regulated by Amount of ADP present


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UPC1 (thermogenin) Brown fat, activated by FA, transports protons from cytosolicside of inner mitochondrial membrane to back intomitochondrial matrix without ATP generation, it uncouples

oxphos which generates heat

Initiation of apoptosis Release of cytochrome C and other proteins into the cytosol

Initial phosphorylation ofglucose

Commitsit to metabolism in the cell

F6P to F6BP Is first committed step in glycolysis

G6P Inhibits hexokinase

PFK1 Rate limiting step, inhibited by ATP and citrate, stimulated by

AMP and F26BP

Pyruvate dehydrogenase Shuttles pyruvate to acetyl coA, inhibited by NADH andAcetyl coA, stimulated by ADP and Ca2+

Pyruvate kinase Pyruvate to lactate, inhibited by ATP, stimulated by F16BP

G3P shuttle Inner mitochondrial membrane is impermeable to NADH,you need a way to get the energy out, works throughDHAP--> G3p which generates FADH2 for ETC

Malate-aspartate shuttle Oxaloacetate cannot cross mitochondrial membrane so it

becomes aspartate which can. It is a cytosolic reducingequivalent both sides make NADH

Increased HIF Increases PFK1c

Cori cycle Shuttles lactate and glucose between the liver andperipheral tissues

Increased NADH Prevents pyruvate oxidation in TCA cycle and directspyruvate to lactate

MEOS Metabolizes ethanol through CYP2E1 P450

Breakdown of ethanol Ethanol-->acetaldehyde-->acetate-->acetyl CoA-->TCAcycle

Homozygous ALDH2*2 Absolute protection against alcoholism, alcoholics aretreated with acetaldehyde dehydrogenase inhibitors


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ADH1B*2 Very fast ADH, associated with decreased alcoholismbecause of negative side effects associated withacetaldehyde accumulations

Highest activity for ethanol CYP2E1, chronic consumption of alcohol increases theselevels and the ER undergoes proliferation

Drinking a little bit,metabolized by...

ADH 1 and ALDH 2

Drinking a lot, metabolizedby

MEOS

Metabolism through ADH Yields more energy!

AST/ALT>1 Acute viral hepatitis

AST/ALT


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Dilichol phosphate Transfers branched sugar chains to amide of nitrogen ofasparagine residues

I Cell Disease Lysosomal enzymes lack mannose 6P marker that targetsthem to lysosomes

Sphingolipids Produced in the golgi

Hexosaminidase A Tests for tay sachs, they will have a decreased amountpresent, accumulate GM2 but nitgloboside

Sandhoff disease Both A and B hexosaminidase are deficient same symptomsas tay sachs with an accelerated time table

apoB48 Intestine

apoB100 Liver

LPL on capillary walls Responds to APO CII on chylomicron to digest TG to FA andglycerol

Remnants Take up through recognition of ApoE

Orlistat Drug that blocks action of pancreatic lipase

MTP inhibitors MPT facilitates making larger B particles by adding lipidsand TG, without this you have abetalipoproteinemia, right

now they have too many bad side effects

ABCA1 Reverse cholesterol transport and biogenisis of HDL, movescholesterol from inner to outer leaflet so that HDL canaccept it, while LCAT helps the HDL trap the cholesterol

RLS of Cholesterolmetabolism

HMG CoA to mevalonate

Regulation of HMGCoA 1. Free cholesterol binds to Scap which inhibits SREBP frombinding to DNA to stimulate transcription of DNA forHMGCoA reductase gene

2. Cholesterol and bile salts increase proteolysis anddegredation of HMGCoA reductase

3. HMGCoA reductase regulated through phosphorylation

ACAT Cholesterol ester production in the liver


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Bile Salt RLS 7 alphahydroxylase, enzyme activity decreased by anincrease in bile salts

Familial HDL deficiency andTangiers disease No ABCA1 so HDL is rapidly degraded

Primary clearance ofcholesterol esters

Scavenger receptor steals esters from HDL then releasesHDL to collect more

LDL receptors reconize ApoB100 or ApoE

Scavenger receptors Not subject to down regulation so they will take up andoxidize more cholesterol developing foam cells

CAH mutation Mutation in 21alphahydroxylase so no aldosterone or

cortisol formation

RLS for Steroid Synthesis CYPIIA: Cholesterol to pregnenalone

Aromatase Formation of estradiol estrone

Vitamin D synthesis 1alphahydroxylase conversion to calcitriol in the kidney

Metformin Decreases blood glucose by inhibiting hepaticgluconeogenesis by activating AMPK through

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One Lines Spring Exam 2