3rd arch: Common carotid arter and proximal internal carotid

4th arch: Left: aortic arch. Right: proximal right subclavian

6th arch: Proximal pulmonary arteries and ducus arteriosus

[image]

What cell wall inhibitor matches the following statement?

• Next step in treatment of otitis media if resistant to amoxicillin

• Prophylaxis against bacterial endocarditis

• Increases the nephrotoxicity of aminoglycosides

• Sufficient for the treatment of syphilis

• Single dose treatment for gonorrhea

• Next step in treatment of otitis media if resistant to amoxicillin: Amoxicillin with Clavulanic acid

• Prophylaxis against bacterial endocarditis

Penicillin V (oral), Aminopenicillins, Ampicillin or 1st generation cephalosporins

• Increases the nephrotoxicity of aminoglycosides

Cephalosporins

• Sufficient for the treatment of syphilis

Penicillin G (IV)

• Single dose treatment for gonorrhea 

Ceftriaxone

caused by failure or disruption in the migration of neural crest cells

Transposition of the great vessels

[image]

Tetrology of Fallot

[image]

Persistent truncus arteriosus

[image]

• Ascending aorta and pulmonary trunk :

Truncus arteriosus

• Coronary sinus: Left horn of sinus venosus

• SVC: Right common and anterior cardinal vein

• Smooth parts of the left and right ventricle: Bulbus Cordis
• Smooth part of the right atrium: Right horn of sinus venosus
• Trabeculated left and right atrium: Primitive Atria

• Trabeculated parts of the left and right ventricle: Primitive ventricle

What structure divides the truncus arteriosus into the aortic and pulmonary trunks?

What is the cellular origin of this structure?

Spiral/ Aorticopulmonary septum

neural crest cells

[image]

Umbilical VEIN

[image]

What causes the foramen ovale and ducts arteriosus to close at birth?

What medication can help close the ducus arteriosus?

at birth the infant takes a breath which decreases pulmonary vasculature resistance and increases left atrial pressure in comparison. This increased pressure causes the foramen ovale to close. The increase in oxygen leads to a decrease in prostaglandins and the ductus arteriosus is closed.

Indomethacin will close it

Prostaglandins E1 and E2 keeps the PDA open

Trisomy 21

[image]

Pyrazinamide

[image][image]

Renal Failure

[image]

Liver dysfunction

CHF

Alcoholism

Always check Serum Creatinine

[image]

Bronchospasm (wheezing)

Right sided heart murmor or lesions

Diarrhea

Flushing

5 T's

Tetrology of Fallot (Pulmonary stenosis→RV Hypertrophy, overriding aorta, VSD)

Transposition of great vessels

Truncus Arteriosus (persistent)

Tricuspid Atresia

Total Anomalous Pulmonary Venous Return (TAPVR)

Trisomy 21

Trisomy 13

Trisomy 18

Cri-du-chat syndrome

The stenotic pulmonic valve causes an increase in pressure causing blood from the right ventricle to flow into the left ventricle throught the ventricular septal defect

[image]

Transposition of the Great vessels

Hypoglycemia

Large for gestational age

(increased risk of clavicle fractures, shoulder dystocia, Erb-Duchenne palsy, failure to progress during delivery)

Ventral Septal Defect

Left to Right Shunt

40% close in first 6 months

Loud S1

Wide, Fixed, Split S2

aortic valve is closing before the pulmonic valve because the pulmonary valve is overloaded with blood

What is infantile coarctation of the aorta?

What genetic syndrome is this associated with?

narrowing of the aorta proximal to the ductus arteriosus

Associated with Turners syndrome.

can cause notching of the ribs

[image][image][image]

aortic coarctation

bicuspid aortic valves-->increased risk of endocarditis

[image][image]

What is Ebstein's anomaly? What causes it?

tricuspid leaflets are displaces into right ventricle, hypoplastic right ventricle, tricuspid regurg or stenosis

caused by maternal Lithium use

[image]

Trisomy 21

AV canal defect leading to ASD, VSD, AVD or all four

[image]

Truncus Arteriosis

Tetrology of Fallot

22q11 defect

[image]

Patent Ductus Arteriosus

Pulmonary artery stenosis

• Chromosome 22q 11 deletions

Truncus arteriosus, Tetrology of Fallot

• Down syndrome

Endocardial cushion defect: ASD,VSD,AVD, or all four

• Congenital rubella

PDA, Pulmonary artery stenosis, septal defect

• Turner's syndrome

Coarctation

• Marfan's syndrome

aortic insufficiency

A 45-year-old male presents with a BP of 160/90 on the right arm and 170/92 on the left arm.

There are no palpable pulses in the feet/ankle.

What problem does this patient most likely have?

Coarctation of the aorta

adult type (distal to ligamentum arteriosum)

Pyruvate Carboxylase

(pyruvate→oxaloacetate)

____________________________

Pep Carboxykinase

(oxaloacetate→PEP)

________________________________

Fructose-1-6-Bisphosphatase

(Fructose-1-6-bisphosphate→Fructose-6-phosphate)

__________________________________________

Glucose-6-Phosphotase

(Glucose-6-phosphate→Glucose)

What cranial nerves innervate the tongue in the following ways?

• Taste in the anterior 2/3
• Taste in posterior 1/3 (main innervation)
• Motor
• Sensation in the anterior 2/3
• Sensation in the posterior 1/3

• Taste in the anterior 2/3

Facial nerve

• Taste in posterior 1/3 (main innervation)

Glossopharyngeal

• Motor

Hypoglossal

• Sensation in the anterior 2/3

Mandibular division of the Trigeminal nerve

• Sensation in the posterior 1/3

Glossopharyngeal

Which tumors arise centrally in the lung and are linked to smoking?

Which tumors arise peripherally in the lung and are less linked to smoking (if at all)?

Central:

Squamous cell and Small cell lung cancer

______________

Peripheral:

Adenocarcinoma and Large Cell carcinoma

MAP=1/3systolic + 2/3diastolic

90=1/3(150)+2/3 diastolic

90=50+2/3diastolic

40=2/3diastolic

120=2(diastolic)

60=diastolic

pulse pressure= systolic-diastolic

150-60=90

90mmHg

Increase contractility:

Digoxin

Catecholamines

Decrease contractilty

Beta blockers

Non-dihydropyridine CCBs

Increase: ↑intracellular Calcium

↓extracellular Na

Increase contractility: ↑intracellular Calcium

↓extracellular Na

____________________________________

Decrease contractilty: acidosis

decrease afterload

decrease contractilty

decrease heart rate

Increased ionotropy/contractility:

-sympathetic stimulation

-Inotropic drugs

-Increasing intracellular Calcium

-Decreasing extracellular Na

afterload

preload

contractility

index of ventricular contractility

EF= SV/EDV

What is the rate limiting of the citric acid cycle?

heavily regulated step?

Isocitrate dehydrogenase os rate limiting

alpha-ketoglutorate dehydrogenase is heavily regulated

Left atrial pressure

measured by a Swan Ganz catheter

ex:

wedge pressure is greater than left ventricular diastolic pressure in the setting of mitral stenosis

[image]

a reduction in circulating RBC mass

resulting in hypoxia and presenting as weakness, fatigue, dyspnea, pale conjunctiva and skin,

possibly headache, lightheadedness, angina (especially with prexisting CAD)

Hgb

Hematocrit

RBC count

each is concentration dependent so can be misleading of the change in RBC mass. For example, a preganant woman's blod volume increases which may cuase her hematocrit and Hgb to go down but her blood cell mass is still normal--only thing that changed was the volume causing dilution. But we use this as a way to determine anemia as best we can

Hgb<13.5 g/dl males

Hgb<12.5 g/dl in females

(can be lower with mestrual cycle)

80-100

below 80= microcytic

above 100=macrocytic

Microcytosis is due to an extra division due to a decreased production of hemoglobin

(think about it like the cells divide more and become smaller to try and maintain that optimal concentration and red color bc there is less hemoglobin)

1-Iron deficiency Anemia (most common type-low iron)

2-Anemia of Chronic disease (inaccessible, this decreased Iron)

3-Sideroblastic Anemia (decreased protoporphyrin)

4-Thalassemia (decreased globin)

duodenum

enterocytes regulate absorption

Why is entry so heavily regulated and bound?

How is it transported and stored in the body?

There is no way for the body to get rid of iron (outside of menses and sloughing the skin)

Iron can create free radicals so it is bound to transferrin in blood to be delivered to liver and bone marrow macrophages for storage

stored in ferrtin within the macrophages

Serum Iron (measures Iron in the blood)

TIBC (measures transferrin molecules in blood)

% saturation (measures bound transferrin molecules in blood)

Serum ferritin (measures stored iron in bone marrow macrophages and liver)

What is the most common cause of Iron deficiency in:

Infants

Children

Adults

Elderly

Infants: breast feeding

Children: Poor diet

Adult males: peptic ulcer disease

Adult femailes: menorrhagia or pregnancy

Elderly: Colon polyps/carcinoma (Western)

Hookworm: majority countries

What happens to ferritin and TIBC during the first stage of iron deficiency?

2nd, 3rd, 4th?

1)↓Ferritin ↑TIBC

storage iron is depleted first causing a decrease of the storage iron protein ferritin in the serum and an increase in the Total Iron Binding Capcity bc the liver pumps put more transferrin to pick up iron

2)Serum Iron ↓and

% saturation↓

less molecules of iron bound to transferrin molecules

3) Normocytic Anemia

initially the bone marrow will just make less, but normal RBCS

4)Microcytic Anemia

In this stage, the iron deficiency becomes so sever, and the bone marrow starts pumping out cells that have undergone more divisions so they will be microcytic and with less hemoglobin ( hypochromic) RBCs

Iron Deficiency

koilonychia:[image]

FEP is Free Erythroctye Protoporphyrin

In thes etting of Iron Deficiency Anemia, the problem is iron not protoporphyrin. Heme is made up of Iron and protoporphyrin so because there isn't enough iron to bind protoporphyrin, there will be an increased amount of free protoporphyrin in the RBC

RBCs should be about the size of the nucleus of a lymphocyte

image of normocytic anemia

[image]

What is the most common anemia in hospitalized patients?

What is the pathogenesis?

Anemia of chronic disease (microcytic anemia)

chronic inflammation causes an increase in an acute phase reactant hepcidin which sequesters iron in storage sites and limits iron transfer from macrophages to erythroid precursors

hepcidin also suppresses EPO production

why?

the body thinks there is a microbe present causing inflammation and it holds onto the iron so that the "invading microorganism" can't use it to divide and be successful in the body. However this happens with chronic diseases that are not due to microbial infection all the time

↑ferritin ↓TIBC

↓serum iron

↓%saturation

↑FEP

decrease inflammatory cause/ inflammation

EPO (especially in cancer patients)

defective protoporphyrin synthesis causing

microcytic anemia

What is the rate limitng step in the formation of protoporphyrin?

What is the enzymes responsible for this step and the next step?

1)ALAS (requires B6)

ALA Synthetase

Succinyl CoA--->ALA

2) ALAD (second step)

ALA-Dehydrogenase

ALA--->Porphobilinogen

the enzyme that catalyzes the joining of Iron and Protoporphyrin to make Heme

takes place in the mitochondria

[image]

Sideroblasts are Erythroid precursors characterized by a ring of iron filled mitochondria surrounding the nucleus called a "ringed sideroblast.

This occurs in the setting of sideroblastic anemia due to deficiency in protoporphyrin.

Iron is transported into the erythroid precursor to bind with protoporphyrin to make heme, but if absent, iron has no way to exit the cell so it accumulates in the mitochondria

congenital: defect in ALAS (Rate limiting enzyme)

acquired: alcoholism (toxic to mitochondria),

lead poisoning (denatures ALAD and ferrochelatase), vitamin B6 deficiency (B6 is required for ALAS

*PHARM TIE IN: Isoniazid can cause a B6 depletion and sideroblastic anemia*

[image]

↑ferritin ↓TIBC

↑serum iron ↑%saturation

similar findings of hemachromatosis bc they are both an "iron overloaded state"

Thalassemia

inherited mutation and carriers are protected against the plasmodium falciparum malaria

4 alpha alleles

chromosome 16

alpha thalassemia: gene deletion

3 alpha genes

1-alpha gene: asymptomatic

2-alpha genes: mild anemia

3-alpha genes: severe anemaia

4-alpha genes: incompatabile with life (hydrops fealis)

Hgb Barts on electrophoresis (tetramer of gamma chains)

β/β+

one normal/ one decreased synthesis

mildest beta thalassemia

asymptomatic

increased HbA2

microcytic. hypochromic anemia with target cells

Which beta thalassemia results in a severe form of anemia a few months after birth?

Why?

βo/βo

presents a few months after birth bc fetal Hgb is α2/γ2 and it persists a little while after birth

but eventually the baby will change to α2/α2 because there is no Beta globulins. The alpha tetramers will precipitate and damage the RBCs causing ineffective erythropoiesis, extravascualr hemolysis due to destruction bythe spleen, and massive erythroid hyperplasia (expansion of hematopoiesis into marrow of skull and facial bones), hepatosplenomegaly, risk of aplastic crisis with parvovirus B19 (Virus that effects the erythroid precursors)

Tx: chronic transfusions which can cause secondary hemochromatosis (iron overload)

Labs: microcytic, hypochromic RBCs and target cells

HbA2 (alpha2 and delta2) and HbF (alpha 2 and gamma 2)  on electrophoresis

NO HbA. WHY?--bc HbA is made up of alpha2 and beta2 which these ppl dont have

crew cut skull

[image]

Chipmunk like face

[image]

What is this image about? How does this relate to anemia?

[image]

The role of Folate, B12 and honocystein in DNA synthesis

1) THF enters the cell and is methylated

2) In order to participate in DNA synthesis it passes along the methyl group to B12

3) B12 passes the methyl group to homocysteine which then becomes methionine

B12.folate deficiency leads to megaloblastic anemia

megaloblasts in rapidly defining cells

hypersegmented neutrophils

increased homocystein

normal methylmalonic acid(if only folate deficiency)

Methylmalonic Acid cannot be converted into Succinyl CoA without B12

Methylmalonic acid will build up in particular within the myelin of the spinal cord and cause degeneration

NOT seen in folate deficiency

peripheral destruction (good marrow response)

-or-

underproduction (poor marrow response)

determined by looking at reticulocytes on blood smear

which looks blue due to RNA in the cytoplasm

inherited defects of the RBC cytoskeleton membrane tethering proteins rendering the cells round instead of biconcave disc shape

most commonly:

spectrin

ankyrin

band 3.1

blebs are broken off and you get an increased RBW

hard to travel through the spleen and are destroyed

extracascular anemia

[image]

splenomegaly (hypertrophy as spleen eats up these RBCs)

jaundice: unconjugated bilirubin overload

increased risk of bilirubin gallstones:conjugated bilirubin overload

increased risk of aplastic crisis with infection of parvovirus B19

Dx: osmotic fragility test

increased fragility in hypotonic solution

Tx: splenectomy

Hypoxemia

Dehydration

Acidosis

polymerization when deoxygenated therefore a reversible reaction

can be irreversible and cause dactylitis: common sign in infants presenting with sickle cell anemia

What is the most common cause of death in children with sickle cell ?

adults with sickle cell?

children:

adults: acute chest syndrome (vasoocclusion in pulmonary microcirculation) precipitated by pneumonia (inducing sickling in the lungs)

children: infection by encapsulated organisms

because they produce less than 50% HbS

50% or more is required for sickling to take place in vivo except in the renal medulla which these ppl can have microinfarctions and lead to a decreased ability to concentrate urine

can check if someone has trait with a metabisulfite screen or electrophoresis

Hemoglobin C has glutamoic acid replaced by lysine

mild anemia

crystals on blood smear

Sickle cell has glutamic acid replaces by valine

thrombosis

because as platelets are lysed the fragments can release cytoplasmic contents into circulation and induce thrombosis

mainly in hepatic, portal or cerebral veins

acquired defect in PIGA gene myeloid cells of Gpi which is required for the expression of CD55(DAF) and MIRL

DAF and MIRL protect RBCs, WBCs and platelts from destruction by complement

At night this occurs in these patients because we normally breath more shallowly at night and are a little respiratory acidic--> this activates complement which normally doesn't have an effect but in these patients the RBCs, WBCs and platelets are lysed

They wake up in the morning with dark urine

labs: hemoglobinema

hemoglobinuria

hemosiderin (days later)

screen: sucrose test

confirm: acidified serum test or flow cytometry to look for CD55

Iron deficiency anemia

10% develop AML (think bc PNH is acquired mutation so you are more likely to acquire other mutations)

reduced half life of the enzyme cuasing a decreased ability to deal with neutralization of H202 in the cell resultin in oxidative stress and damage

causes intravascular hemolysys

due to infections, drugs (primaquine, sulfa drugs, dapsone), and fava beans

African variant: mild reduction in half life

Mediterranean variant: markedly reduced half life

enzyme studies confirm diagnosis--can only be done after the crisis

IgG 37 degrees celsius

SLE

RA

CLL

IgM and C3b

4 degrees celsius

warm body centers

Mononucleosis

Mycoplasma pneumonia

Raynauds Phenomenon

nonspecific inflammatory sympoms: fever, athralgia,fatigue, weight loss etc..

organ ischemia symptoms based on the vasculitis

(endothelium is damaged resulting in thrombis and/or inflammation followed by healing and fibrosis narrowing the lumen)

most are not infectious

Kawasaki's disease

Aspirin and IVIG are teatment to protect them against thrombus in coronary artery

only time bc aspirin is toxic to children

necrotizing vascultitis involving the digits

Raynaud's phenomenon is often pressent

highly associated with smoking

[image]

"Wecener's"

 the C disease

 c-ANCA

Necrotizing granulomatous vascultis involving NASOPHARYNX, LUNGS, KIDNEY

[image]

sinusitis, ulcers in the nasopharynx, hemoptysis with bilateral lung infiltrates, hematuria due to RPGN

[image]

relapses are common

Tx Cyclophosphamide

necrotizing vascultits

lung and kidney involvement

p-ANCA

like wegeners but

NO GRANULOMAS

NO NASOPHARYNGEAL INVOLVEMENT

p-ANCA

Asthma

peripheral eosinophilia

granulomatous necrotizing vasculitis

increased plasma renin

atrophy of affected kidney

caused by

atherosclerosis (older males)

fibromuscular dysplasia (young female)

Intimal plaque that obstructs blood flow

cholesterol with fibromuscular cap

involves large and medium arteries

abdominal, coronary, popliteal and internal carotids

[image]

When do you usually see symptoms of atherosclerosis?

What are the 4 complications of atherosclerosis?

greater than 70% stenosis

Stenosis:

PVD (EX.popluteal artery)

Angina (coronary artery)

Ischemic bowel disease (mesenteric artery)

other complications

Plaque rupture with thrombosis

MI (coronary artery)

Stroke (middle cerebral artery)

Plaque rupture with embolization

atherosclerotic emboli with cholesterol clefts

Weakining of the vessel wall

aneurysm (abdominal aorta ex.)

ppl with benign HTN

(due to high pressures forcing proteins in)

ppl with Diabetes

(due to nonenzymatic glycosylation of basement membrane making wall leaky and protein comes in)

proteins leaking through vascular wall and organizing as hyaline membane around the lumen

[image]

results in ischemia especially to the kidney (glomerular scarring) and eventual renal failure

arteriolonephrosclerosis

[image]

Malignant HTN

Onion skin appearance

and narrowing of the lumen

may lead to fibrinoid necrosis and end organ ischemia especially kidney (renal failure) with flea bitten appearance

[image]

[image]

What is this a picture of?

Aortic dissection

occurs in proximal 10 cm of aorta (high pressure)

with pre-existing weakness of the media

commonly due to:

most common in HTN (hyaline arteriosclerosis of the arteries in he vaso vasorum of the adventitia)

inherited defect of connective tissue (Marfan's:fibrillin defect, also Ehler's Danlos: defective collagen)

presentation: sharp tearing chest pain that tears to the back and commonly causes pericardial tamponade that leads to death

can also rupture out into the mediastinum

or tear down the aortic intima and compress the renal artery

What is the classic cause of thoracic aneurysm?

complications?

weakening of the aortic wall due to tertiary syphillis

with a tree bark apearance of the aorta

[image]

complications:

-dilation of the aortic valve root with insufficiency resulting in aortic insufficicency

-thrombosis-->thomboemboli

atherosclerosis

classically male smokers over 60 yo with HTN

pulsatile abdominal mass that grows with time

rupture at greatest risk >5cm in diameter

rupture triad: hypotension

pulsatime abdominal mass

flank pain

[image]

[image]

Gel electrophoresis and blot is formed on HIV protein standards

Blot is incubated with the patient's serum

Presence of anti-HIV antibodies in serum are detected

deficienct in G6PD generate NADPH which produces reduced glutathione

without the enzyme, RBCs are more susceptible to  oxidative damage and hemolysis

How do the following circumstances impact the Starling forces of fluid movement through capillaries?
• Heart failure
• Liver failure
• Renal failure
• Infections and toxins
• Nephrotic syndrome
• Lymphatic blockage
• Bums
• Diuretic administration
• IV infusion of albumin or clotting factors

• Venous insufficiency

• Heart failure

increased capillary pressure

• Liver failure

decreased oncotic pressure

• Renal failure

decreased plasma protein, decreased plasma colloid osmotic pressure

• Infections and toxins

increased capillary permeability

• Nephrotic syndrome

increased plasma protein and decreased plasma colloid osmotic pressure

• Lymphatic blockage

increased osmotic pressure *nonpitting edema*

• Burns

increased capillary permeabilityums

• Diuretic administration

osmotic agent that prevents water reabsorption

• IV infusion of albumin or clotting factors

increase plasma proteins and increase plasma colloid osmotic pressure

• Venous insufficiency -increased capillary pressure

Lateral to medial to find the NAVEL

Nerve Artery Vein Lymphatics

femoral nerve is outside the femoral sheath

[image]

A sound heard in early diastole due to rapid ventricular filling

more common in dilated ventricles (CHF, dilated cardiomyopathy, mitral regurg, increased filling pressures, left to right shunting (VSD, ASD, PDA))

but considered normal in children and pregnant women

[image]

the atrial kick that occurs in late diastole due to high atrial pressure associated with ventricular hypertrophy

(aortic stenosis, hypertrophic cardiomyopathy, chronic hypertension, common after MI)

[image]

S3 whether the ventricles are dilated

 (early diastole)

_________________________________________

S4 whether the ventricles/valves are stiff

(late diastole)

during inspiration over the pulmonic region

[image]

caused when the closure of the aortic valve and pulmonic valve are not synchronized

If you hear persisitent fixed splitting throughout the cycle in other regions of the chest, consider

pulmonary hypertension

atrial septal defect

right heart failure

split only during expiration (paradoxical):

aortic stenosis, hypertrophic cardiomyopathy, left bundle branch block and ventricular pacemaker (reverse splitting)

wide splitting with expiration:

pulmonic stenosis, right bundle branch block

http://www.bing.com/videos/search?q=splitting+heart+sounds&FORM=HDRSC3#view=detail&mid=437174925C45638C5CAB437174925C45638C5CAB

a : atrial contraction

c:ventricular contraction

v:atrial filing with a closed tricuspid valve

This shunt reversal is called Eisenmenger Syndrome and is a large Septal defects

In the beginning, blood from the Left ventricle (high pressure) will preferentially move to the right ventricle (low pressure) creating a left to right shunt.

Over time, because the right side is so overloaded with blood and the pressure, pulmonary hypertension will develop.

The pressure on the right side will exceed that pf the left and blood from the right ventricle (deoxy) will move over to the left side of the heart and into systemic circulation resulting in cyanosis and a right to left shunt

[image]

Ostium primum ASD

split S2 on auscultation bc the right side is getting extra volume resulting in delayed closure of the pulmonic valve

(Ostium secundum is the most common type however)

Patent Ductus Arteriosus

eisenmeger syndrome with lower extremeity cyanosis happens later on in the progression if not treated with Indomethicin

[image]

assoc. with congenital rubella

Ts

Tetralogy of Fallot

Tricuspid Atresia

Truncus Arteriosus

Transposition of the Great Vessels

scarring of the aortic valve with fusion of the commisures with mitral stenosis.

What caused this and what murmur is associated with the aortic stenosis?

chronic rheumatic valve disease

systolic ejection click followed by

crescendo-decrescendo murmur

[image]

concentric left ventricular hypertrophy

angina and syncope with exercise

microangiopathic hemolytic anemia

Aortic regurg is backflow of blood from aorta into LV duing diastole

most common cause is aortic root dilation (syphilitic aneurysm) or valve damage from infectious endocarditis

[image]

aortic regurgitation

diastolic decrescendo murmur

widening pulse pressure/hyperdynamic circulation causes the bounding pulses, head bobbing, and pulsating nail bed

Clinical features:

LV dilation and eccentric hypertrophy

[image]

https://www.youtube.com/watch?v=IfJotUSNgdo

complication of MVP

LV dilation

infective endocarditis

acute rheumatic heart disease

papillary muscle rupture after MI

how do these effect valves:

chronic rheumatic disease___

acute rheumatic disease___

chronic: stenosis

acute: regurgitation

AS (radiates to neck)

MVP (click, increases with valsalve)

HOCM (increases with valsalva move)

[image]

MR

(high pitched blowing, increases with increased TPR : squatting and handgrip or increased LA return: expiration,radiates to axilla)

_______________________________________

TR

(high pitched blowing, increase w/ RA return- inspiration increases)

______________________________________

VSD

(harsh)

AR

best heard LSB with patient leaning forward

high pitched blowing heard at the end of expiration

[image]

MS

opening snap due to tensing of chordae tenidinae

increases with increase LA pressure: expiration

late diastolic rumble heard best at the apex in left decubitus position

NO RADIATION

assoc. with rheumatic fever

Nagging Pests Must Breath

Nocardia

Pseudomonas

Mycobacterium tuberculosis

Bacillus species

MVP

HOCM

Aortic stenosis

(no murmur at the beginning of systole, ejection click is the popping of the aortal valve open)

S1-ejection click-crescendo-decrescendo-S2

Radiates to carotid

weak pulses and syncope

holosystolic murmur

loudest on inspiration

tricuspid regurgitation (IV drug user)

VSD (infant)

Bicuspid Valve

Unicuspid valve

Aging-Calficiation

Chronic Rheumatic Heart Disease

Syncope

weak pulsus

harsh crescendo-decrescendosystolic ejection murmur

radiating to carotids

mitral stenosis

OS/MS

Mitral Stenosis

Mitral regur and stenosis

left sided S3 and S4

Strep viridans

low virulence: small vegetations, but act as a trap for transient bacteria

Staph Aureus

high virulence: infects normal valves

large vegetations-->acute endocarditis

tricuspid valve

HACEK organisms

Haemophilus,

Actinobacillus,

Cardiobacterium,

Eikenella,

Kingella

very hard to grow

Fever

Murmur

Janeway Lesions (septic emboli-painLess)

Osler nodes (septim emboli-painful Ouch)

Anemia of chronic disease

[image]

Libman-Sacks Endocarditis

results in mitral regurgitation

Idiopathic

Genetic Mutation (AD)

Myocarditis

Drugs (Doxorubicin, Cocaine)

Alcohol abuse

Pregnancy (late 3rd trimester, soon after birth)

Coxsackie Virus B

tx:transplant

genetic mutations in sarcomere proteins causing disorganized fibers and massive hypertrophy of the left ventricle

 [image]

most common cause of sudden death in young athletes

[image]

Hypertrophic cardiomyopathy

[image]

What causes restrictive cardiomyopathy?

How does it present on EKG?

amloidosis

sarcoidosis

hemochromatosis

endocardial fibroelastosis(children)

Loeffler syndrome (eosinophilc infiltrate causing fibrosis)

presents as CHF

low voltage EKG with diminished QRS

Myxoma

most common primary cardiac tumor in adults

Rhabdomyoma

benign hamartoma of cardiac muscle

usually arises in ventricle

breast, lung,melanoma, lymphoma

pericardium

causing pericardial effusion

- Mildly decreased UDPGT

Gilbert's syndrome

Crigler Najjar Type 2

-Completely absent UDPGT

Crigler Najjar Type 1

- Grossly black liver

Dubin Johnson Syndrome

-Responds to phenobarbital

Gilbert's Syndrome

Crigler-Najjar Type 2

- Treatment includes plasmapheresis and phototherapy

Crigler Najjar Type I

-Asymptomatic unless under physical stress (alcohol, infection)

Gilbert's Syndrome

disulfuram like reaction: inhibition of acetaldehyde dehydrogenase so alcohol cannot be fully metablized

flushing, sweating, nausea, headache, hypotension

Meds:

Metronidazole

Cephalosporins (Cefotetan, Cefamandole, Cefoperazone)

1st gen Sulfonylureas (Tolbutamide)

Phase 0,  by blocking NA channels these anti-arrhythmics are prolonging phase 0 and thus increasing the refractory period which slows the heart down

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Phase 3, these anti-arrhythmics work by blocking K you can prolong the refractory period and slow the heart.

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Calcium channel openining

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Beta blockers decrease the slope of Phase 4 which slows the heart

Calcium channel blockers work on phase 0 here to increase the time required to reach threshold and slowing heart

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The gradual increase of sodium conductance of Phase 4

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No BadBoy Keeps Clean

Class I: Na channel blockers

Class II: Beta Blockers

Class III: K channel blockers

Class IV: Calcium channel blockers

Double Quarter Pounder

Disopyramide

Procainimide  (drug induced Lupus anti-histone)

Quinidine (torsades de pointes, thrombocytopenia)

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What are the Class IB Antiarrhythmics?

Lettuce Tomato Mexican Pickles

most commonly used antiarrhythmics!

Lidocaine (tachyarrhthmias after MI)

Tocanide

Mexelitine

Phenytoin (also an anticonvulsant)

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More Fries Please

not commonly used

Moricizine

Flecanide

Propafenone

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Class II:Beta blockers

decrease cAMP, decrease Ca and suppress slope 4

lol

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Propanolol

Atenolol

Metoprolol

Esmolol (most short acting-V-tac, a fib and A-flutter)

mask the effects of hypoglycemia,exacerbate asthma, bradycardia, AV block, CNS effects

overdose treatment: Glucagon

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Class III: K channel blackers, work at phase 3, elongates refractory period

SAD

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Sotalol

Amiodarone (WPW)

Dofetilide

A-fib, A-flutter

Amidoarone SE: Pulmonary fibrosis, heapotoxicity,hypo-,hyperthyroidism, BLUE-GREY skin discoloration, photodermatitis, corneal deposists, heart failure, has effects of all the classes so always check: PFTs, TFTs, LFTs

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Class IV: Calcium channel blockers, decrease slope of Phase 0: VD

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Verapamil

Diltiazem

Nondihydroperodines

Constipation, flushing, edema, heart failure, dont combine with beta blockers

SVT

short acting drug that increases potassium leaving the cell and decreases permeability of calcium

so there is no depolarization

stops the heart for 5 seconds an starts the heart at a slower heart rate to diagnose SVT

very uncomfortable for patient

Flushing, hypotension, chest pain

Label

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0:Na influx (rapid depolarization)

1:K and Cl efflux (KClout)

2:Ca influx (plateau)

3:K efflux (Kout) (repolarization)

4: K permeability increases

increases them

acidoses is always associated with hyperkalemia

increased sodium causes sodium to enter the cells (down the gradient) and therefore K will be pushed out

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Treat: Calcium and Bicarb especially when somone is coded for a long time

Quinidine

IA

Delta waves

syndrome of preexcitation of ventricles of the heart

from bundle of kent

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What are the two different types of second degree AV block?

How do they differ?

Mobitz Type I (Wenkebach gives a warning)

progressively prolonged PR intervals , then a blocked beat

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Mobitz Type II

blocked beat without the progressive PR prolongation

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Narrow:

conducted through the normal pathway

Wide:

NOT CONDUCTED normally through normal conduction pathway

What is the ECG axis given the QRS deflections in the following scenarios?
• Positive in lead I, positive in lead II

• Positive in lead I, negative in lead III

• Negative in lead I, positive in lead III

• Positive in lead I, negative in aVR

• Positive in lead I, positive in lead II

Normal axis

• Positive in lead I, negative in lead III

Left axis deviation

• Negative in lead I, positive in lead III

Right axis deviation

• Positive in lead I, negative in aVR

Normal Axis

What is the treatment for ventricular fibrillation?

No correlation between P waves and QRS

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Macrolides

Haloperidol

Chloroquine

Risperodone

Class IA Antiarrhythmics

Class III Antiarrhythmics

Protease Inhibitors

PBC: autoimmune associated with CREST scleroderma

positive AMA, middle aged women

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SC:unknown etiology, p-ANCA

middle aged men, associated with ulcerative colitis

ERCP: alternating beads and stricturing

What substances act on smooth muscle myosin light-chain kinase?

How does this effect blood pressure?

Dihyroperidone

Calcium channel blockers

Epinephrine (B2 receptors)

Prostaglandin E2

Relax vascular smooth muscle ---> decrease BP

Beta blocker

mediastinal widening on chest xray

HTN: >140/90

PreHTN: 120-139/80-89

What would you most suspect the cause of hypertension to be in a patient with the following
clinical clues?

• Paroxysms of increased sympathetic tone: anxiety, palpitations, diaphoresis

• Age of onset between 20 and 50

• Elevated serum creatinine and abnormal urinalysis

• Abdominal bruit

• BP in arms > legs

• Family history of HTN

• Tachycardia, heat intolerance, diarrhea

• Hyperkalemia

• Episodic sweating and tachycardia

• Abrupt onset in a patient younger than 20 or older

than 50, and depressed serum K levels

• Central obesity, moon-shaped face, hirsutism

• Normal urinalysis and normal serum K levels

• Young individual with acute onset tachycardia

• Hypokalemia
• Proteinuria

• Paroxysms of increased sympathetic tone: anxiety, palpitations, diaphoresis: Pheochromocytoma

• Age of onset between 20 and 50: Primary HTN

• Elevated serum creatinine and abnormal urinalysis: Renal disease

• Abdominal bruit: Renal artery stenosis

• BP in arms > legs: Coarctation of the aorta

• Family history of HTN: Primary HTN

• Tachycardia, heat intolerance, diarrhea: Hyperthyroidism

• Hyperkalemia: Renal failure

• Episodic sweating and tachycardia: Pheochromocytoma

• Abrupt onset in a patient younger than 20 or older than 50, and depressed serum K levels:Hyperaldosteronemia

• Central obesity, moon-shaped face, hirsutism: Cushing Syndrome

• Normal urinalysis and normal serum K levels: Primary HTN

• Young individual with acute onset tachycardia: Cocaine or amphetamines

• Hypokalemia : Renal artery stenosis

• Proteinuria: Renal disease

Cardiomyopathy

Cardiomyopathies are noninflammatory myocardial disorders that are not associated with coronary artery obstruction, hypertension, valvular disease, congenital
heart disease, or infectious disease. They are most often characterized by otherwise unexplained ventricular dysfunction, such as cardiac failure, ventricular enlargement, or ventricular arrhythmias.

Uremia due to renal failure

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Myasthenia Gravis

Neostigmine (post op neurogenic ileus too)

Pyridostigmine

Atropine overdose

Physiostigmine

Diagnose MG:

Edrophonium

Glaucoma

Echotiphate

Alzheimers:

Donepizil

Galantamine

Rivastigmine

Organophosphaste:

Parathion

Troponin

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