Nycc Seva Philomen Md Visceral Path Ex 1

Front 1

Question

Back 1

Answer

Front 2

2 increases with HYPERTROPHY of heart?

Back 2

Hypertrophy is an increase in SIZE, not in number, and an accumulation of SARCOMERE PROTEINS.

Front 3

What does hypertrophy initially reflect and what occurs with steady stress?

Back 3

Initially: a compensatory and potentially reversible mechanism (Exercise) but with persistent stress myocardium becomes irreversibly enlarged and dilated (hypertension)

Front 4

Patient presents with hypertension, enlargement of myocytes, right-sided heart failure, stenosis of valves, thickening of myocardium. Condition?

Back 4

CONCENTRIC hypertrophy

No dilation of chamber walls, just of the myocardium itself. This blows the valves, causing them to harden to withstand the pressure. The right side of the heart, smaller than the left to begin with, is now almost without a chamber due to the huge myocytes.
Concentric hypertrophy is like growing from the outside in with no extra room.

Front 5

What is ECCENTRIC hypertrophy and what are risk factors?

*eccentric, regurgitating incompetents

Back 5

eccentric, regurgitating incompetents

ENLARGEMENTof cardiocytes -
thicker myocardium w/ DILATION OF CHAMBER (ventricle)

** REGURGITATION or INCOMPETENCE because ventricles so enlarged the valves aren't made to take that volume or stretch (AI and PI)

Front 6

CONGESTIVE heart failure?

Back 6

ACCUMULATION of blood; unable to pump out.

The term "heart failure" is sometimes incorrectly used to describe other cardiac-related illnesses, such as myocardial infarction (heart attack) or cardiac arrest.~WIKI

Front 7

heart FAILURE causes (5)

Back 7

1. weak ventricular CONTRACTION
2. abnormal ventricular RELAXATION
3. outflow OBSTRUCTION
4. weak MUSCLE
5. increased WORK due to PRESSURE or VOLUME OVERLOAD

Front 8

What side of the heart is affected with backward failure?

Back 8

Right sided heart failure

the right has backward thinking -fail!

Front 9

What side of the heart is affected with forward failure?

Back 9

Left sided heart failure = forward fail

THE LEFT IS FORWARD THINKING

Front 10

3 FETAL SHUNTS

Back 10

DUCTUS ARTERIOSIS

DUCTUS VENOSUS

FORAMEN OVALE

Front 11

What is the most common condition responsible for cardiac failure (accounts for 80% of heart disease deaths)?

Back 11

ISCHEMIA ( CORONARY ARTERY DISEASE)

The remaining 20% are caused by heart muscle disease and congenital heart diseases

Front 12

ductus arteriosis

Back 12

a shunt connecting the pulmonary artery to the aortic arch. It allows most of the blood from the right ventricle to bypass the fetus's fluid-filled lungs.

Front 13

Do we get signs or symptoms with Left Ventricular Failure?

Back 13

SYMPATHY WITH THE LEFT!
LVF = symptoms (sympathy)

RVF = signs

Front 14

Usually, the DA begins to close when breathing is established, and is completely sealed after four to ten days. A cord-like vestige of the DA, called the _____________ _______________, remains to connect the exterior of the left pulmonary artery to the exterior of the aortic arch.

Back 14

ligamentum arteriosum

Front 15

ETIOLOGY of LEFT fail?

LHIVd

Back 15

etiology = LHIVd
L-EFT
H-YPERTENSION
I-SCHEMIC heart disease
V-ALVULAR d-isease (low %age)

Front 16

a type of valvular heart disease characterized by an abnormal narrowing of the aortic valve opening

Back 16

Aortic Valve Stenosis

Front 17

FAILURE of a child's DA to close after birth

Back 17

PATENT DUCTUS ARTERIOSIS

*LEADS TO LEFT TO RIGHT SHUNT.
DA is maintained by prostaglandins so giving mother ibuprofen will close fetus' DA

Front 18

3 types of AORTIC valvular stenoses:

ARCS

Back 18

ARCS
Aortic = Rheumatic, Congenital, Senile

Front 19

What are clinical features of LHF?

Alas, all that I had HOP'D twere but vain symptoms left by my failing heart.

Back 19

Hemoptysis
Othopnea
Paroxysmal Nocturnal Dyspnea
Dyspnea on exertion (b/c decreased Cardiac Output)

Front 20

typically consists of three leaflets (trileaflets). It mediates the flow of blood from the left ventricle to the aorta and the rest of the body during ventricular systole

Back 20

Aortic VALVE

Front 21

a congenital condition whereby the aorta narrows in the area where the ductus arteriosus (ligamentum arteriosum after regression) inserts.

"contracted, compact. Opposed to effuse. Cylindrical pupa shape"

Back 21

CO-ARC-TATION of Aorta (COA)

coarctate - contracted; compact; opposed to effuse; (metamorphose) that species of change in which the pupa assumes a cylindrical shape, all the members of the body being concealed as in the family of Hippobosca.

Front 22

Initially, the left ventricle compensates by THICKENING of its walls (myocardial hypertrophy) in order to maintain adequate systolic function (pumping pressure) to overcome the increased afterload caused by the STENOTIC AORTIC VALVE. Is there dilation of the chamber or not?

Back 22

CONCENTRIC hypertrophy of AORTIC VALVE STENOSIS

*CON is NO Chamber dilation (but yes to thicker myocardium)

Front 23

What happens to the heart and lungs during left heart failure?

Back 23

LEFT ATRIAL pressure increases

PULMONARY VENOUS pressures increaseS

Lung gets congested "WET" congested capillaries in the alveolar SEPTUM

Heart failure cells/ HEMOSIDERIN-LADEN MACROPHAGES macrophages (HLM)

Front 24

_____________valve stenosis is CONGENITAL = 40-50 yrs

versus
_____________valve stenosis is SENILE = 60-80 yrs

Back 24

MITRAL/BICUSPID valve stenosis is CONGENITAL = 40-50 yrs

AORTIC valve stenosis is SENILE = 60-80 yrs

Front 25

a subset of cells found in the developing heart tube that WILL GIVE RISE TO the heart's VALVES & SEPTA critical to the proper formation of a four-chambered heart.

Back 25

Endocardial CUSHIONS

Front 26

Stenosis of the __________ valve is due to patient having had rheuMatic fever as a child.
[acyanotic]

Back 26

Mitral=rheuMatic


ARCS is Aortic-Rheumatic, Congenital, or Senile

Front 27

Describe LSHF patient ROS:

Back 27

Heart: hypertrophy of LV due to pulmonary resistance/hypertension

Lungs: drowning lungs with Hemosiderin Laden Macrophages

Kidney: decreased blood supply due to lower cardiac output, decreased perfusion, decreased urine production, smaller in size

Brain: inadequate cerebral perfusion due to lowered cardiac output

Muscle: decreased perfusion due to not enough oxygen nor blood itself of m. leads to fatigue and weakness.

Front 28

Heart failure (left or right) has acyanotic AORTIC stenosis involvement?

What are the clinical signs of this kind of heart failure due to stenosis of the aortic valve or the mitral valve?

Back 28

LEFT sided heart failure involves ARCS (Aorta = Rheumatic, Congenital, Senile)
When the aortic valve (senile) or the mitral valve (rheumatic and congenital) are stenosed, they are rigid and hard to open.

~PULMONARY EDEMA due to LVH pushing blood up the down staircase, ie into the pulmonary vein and then back into the lung,
~WEAK S2, because S2 is the sound of the pulmonary valve and aortic valve closing after systole to allow heart to fill.
~SYNCOPE due to lack of cerebral perfusion
~ANGINA due to fibrillation or palpitation b/c heart not getting enough oxygen itself!

Front 29

Reasons (etiology) for RIGHT sided heart failure:

Back 29

1. LEFT side causes it

2. PULMONARY HYPERTENSION Inc. pressure in pulmonary artery (R), pulmonary vein (left) or capillaries (meeting)

3. COR PULMONALE - the lungs themselves are sick (COPD or emphysema)

Front 30

Why would AORTIC STENOSIS cause ANGINA?

Back 30

Remember,a patient will complain of pain and symptoms are LVF: Angina in the setting of AS is secondary to the left ventricular hypertrophy (LVH) that is caused by the constant production of increased pressure required to overcome the pressure gradient caused by the AS [wiki]

Front 31

Pressure compensation areas for RSHF?

Back 31

RIGHT ATRIUM &
SYSTEMIC VENOUS (superior and inferior vena cavas)

Front 32

The ischemia may first be evident during exercise, when the heart muscle requires increased blood supply to compensate for the increased workload. The individual may complain of exertional _______

Back 32

angina due to aortic stenosis

*and stenosis of coronary artery

Front 33

What are CLINICAL SIGNS of RIGHT VENTRICULAR FAILURE and the 4 seen first? There are 7 total signs.

In other words, what do you see on your patient w/ RVF?

Back 33

1. DISTENTION of neck veins
2. Elevated JUGULAR venous pressure
3. HEPATOMEGALY and tender liver
4. Peripheral PITTING EDEMA

ENLARGED SPLEEN
Hepato-abdomino-jugular REFLEX
ASCITES

Front 34

Why does the SUBENDOCARDIUM become ischemic first?

Back 34

The subendocardium is the region that becomes ischemic because it is the most distant from the epicardial coronary arteries.[wiki]

Front 35

What is DIASTOLIC heart failure?
(ie, what has happened to the ventricle to make it fail on filling/relaxation?)

Back 35

STIFF VENTRICLE

Need greater pressure to fill (diastolic)
YOU'RE TOO STIFF; YOU CAN'T RELAX!

may exhibit normal size and systole

Front 36

There may also be a noticeable delay between the first heart sound (on auscultation) and the corresponding pulse in the carotid artery (so-called 'apical-carotid delay')

Back 36

aortic stenosis because of pressure required to open stenotic aortic, there is a delay - it takes longer to force the door open

[wiki]

Front 37

Name for the stiffening or hardening of the ventricles (microscopic presentation) for DIASTOLIC heart fail

Back 37

INTERSTITIAL FIBROSIS
causing decreased compliance of ventricular myocardium.

Front 38

The second heart sound (A2) tends to become decreased and softer as the ____________ becomes more severe. This is a result of the increasing calcification of the valve preventing it from "snapping" shut and producing a sharp, loud sound

Back 38

aortic stenosis

weak S2

Front 39

What is congenital heart disease and its prevalence?

Back 39

Results from faulty embryonic development. 7 per 1000

Front 40

is a congenital heart defect in which the opening of the tricuspid valve is displaced towards the apex of the right ventricle of the heart.

Back 40

EBSTEIN malformation/anomaly

[wiki]

Front 41

congenital heart defect that enables blood flow between the left and right atria via the interatrial septum

Back 41

ASD (Atrial Septal Defect)

Front 42

What can be causes of congenital heart disease?

Back 42

Genetic, Chromosomal anomalies (Turners and Downs), Maternal rubella infection, alcohol/ecstacy abuse, drugs in early pregnancy and maternal diabetes

Front 43

the tissue that divides the right and left atria.

Back 43

interatrial septum

Front 44

valve anomaly of EBSTEIN


Ebstein had a regurgitating _______
And by his own swollen ankles was disgusted.

Back 44

TRICUSPID

Ebstein had a regurgitating _______
And by his own swollen ankles was disgusted.

allows backflow b/w R atrium and R ventricle

Front 45

Without this septum, or if there is a defect in this septum, it is possible for blood to travel from the left side of the heart to the right side of the heart, or vice versa.[1] This results in the mixing of arterial and venous blood, which may or may not be clinically significant. This mixture of blood may or may not result in what is known as a "shunt"

Back 45

ASD: (of cyanose tardive) The amount of shunting present, if any, dictates hemodynamic significance. A "right-to-left-shunt" typically poses the more dangerous scenario

Front 46

What are types of congenital heart disease? (8)

Back 46

1. MC: ventricular septal defects 2. atrial septal defects 3. patent ductus arteriosus 4. tetralogy of fallot 5. pulmonary stenosis 6. coarctation of the aorta 7. aortic stenosis 8. complete transposition of the great aa.

Front 47

During development of the fetus, the interatrial septum develops to separate the left and right atrium. However, the foramen ovale (pronounced /fɒˈreɪmən oʊˈvɑːliː/) allows blood from the right atrium to the left atrium during fetal development.

Back 47

FORAMEN OVALE: This opening allows blood to bypass the nonfunctional fetal lungs when the fetus obtains its oxygen from the placenta.

Front 48

the process in which a left-to-right shunt caused by a congenital heart defect causes increased flow through the pulmonary vasculature, causing pulmonary hypertension, which in turn, causes increased pressures in the right side of the heart and reversal of the shunt into a right-to-left shunt.

Back 48

EISENMENGER'S COMPLEX

[wiki]

Front 49

Describe the acyanotic group of congenital heart disease.

*think: what two defects are after the lung entrance or exit? So they would not have much to do with oxygen.

Back 49

COARCTATION OF AORTA
AORTIC STENOSIS

No shunt and no cyanosis: abnormal passage/flow of blood DUE TO CONSTRICTION of some sort

Front 50

Acts as a valve over the foramen ovale during fetal development. After birth, the pressure in the pulmonary circulatory system drops, thus causing the foramen ovale to close entirely.

Back 50

SEPTUM PRIMUM

In approximately 25% of adults,[2] the foramen ovale does not entirely seal.[3] In this case, elevation of pressure in the pulmonary circulatory system (i.e.: pulmonary hypertension due to various causes, or transiently during a cough) can cause the foramen ovale to remain open. This is known as a patent foramen ovale (PFO).

Front 51

EISENMENGER

Back 51

the process in which a left-to-right shunt caused by a congenital heart defect causes increased flow through the pulmonary vasculature, causing pulmonary hypertension, which in turn, causes increased pressures in the right side of the heart and reversal of the shunt into a right-to-left shunt.

Front 52

Any process that increases the pressure in the _______ ventricle can cause worsening of the left-to-right shunt.

Back 52

LEFT

Front 53

Describe the cyanose tardive group of congenital heart disease.

Back 53

An initial L-R shunt w/ late reversal of flow; d/t patent ductus arteriosus, atrial septal defect, ventricular septal defect. Cyanosis supervenes later, shunt L-R then goes R-L b/c increases in resistance cause R vent. pressure to exceed that of L vent.

Front 54

why RIGHT ventricle hypertrophy during ASD?

Back 54

Right v. has to push out more blood due to left>right shunt

Front 55

why called CYANOSE TARDIVE?

Back 55

fancy way of saying late cyanosis- develops AFTER reversal of flow (L-R becomes R-L)
and causes body to be supplied w/ DE-OXYGENATED blood

Front 56

The right ventricle will be forced to generate higher pressures to try to overcome the pulmonary hypertension due to an _____

Back 56

ASD:

"pulmonary hypertension" was clue.

Front 57

Describe the cyanotic group of congenital heart disease.

Back 57

Born with R>l shunt, it doesn't 'develop' over time.

Includes TETROLOGY OF FALLOT and COMPLETE TRANSPOSITION of great vessels with atrioventricular accordance. .

Front 58

what happens If left uncorrected, the pressure in the right side of the heart will be greater than the left side of the heart. This will cause the pressure in the right atrium to be higher than the pressure in the left atrium.

Back 58

EISENMENGERS:
This will reverse the pressure gradient across the ASD, and the shunt will reverse; a right-to-left shunt will exist.

Front 59

In ADULTS, the most common causes of CYANOTIC CONGENITAL heart disease are

Back 59

EISENMENGER syndrome and TETROLOGY OF FALLOT


Eisenmenger's syndrome specifically refers to the combination of systemic-to-pulmonary communication, pulmonary vascular disease and cyanosis & is CYANOSE TARDIVE

Front 60

why does TARDIVE CYANOSIS finally appear w/ ASD?

Back 60

Once TARDIVE right-to-left shunting occurs, a portion of the oxygen-poor blood will get shunted to the left side of the heart and ejected to the peripheral vascular system. This will cause signs of cyanosis.

Front 61

SHUNT categories of congestive heart failure (3)

Back 61

Left > Right shunt
Right > Left shunt
NO shunt

Front 62

the most common type of atrial septal defect

Back 62

ostium secundum atrial septal defect

Front 63

A number of congenital heart defects can cause Eisenmenger syndrome, including (3)

Back 63

ASD
VSD
PDA

*all start left to right but can eventually switch to right to left shunt when right ventricle finally is hypertrophic enough to overpower the normally stronger left ventricle. Then deoxygenated blood is pumped into the circulation and PHTN sx show up.

Front 64

LUTENBACHER syndrome

Back 64

LUTENBACHER:
Ten to twenty percent of individuals with ostium secundum ASDs also have ________valve prolapse DUE TO STENOSIS.


MITRAL V. STENOSIS + ASD = Lutenbacher

Front 65

What condition(s) can be included in Lt - Rt CHD?

Back 65

ASD VSD PDA

Front 66

ATYPICAL angina SPASM (due to cocaine, etc.) that occurs at rest

Back 66

PRINZMETAL ANGINA (VARIANT ANGINA)

Not due to atherosclerosis

coronary arteries are structurally normal - just spasm

Front 67

there is a fixed splitting of S2 =

Back 67

ASD, there is a fixed splitting of S2

*because if there is Eisenmenger reverse and the shunt is now R>L, the extra pressure on the aortic valve must cause it to fire early (or late, I don't know. It just doesn't slap shut when the pulmonary valve does like it's supposed to)

Front 68

the vasodilator works ________

Back 68

everywhere, even though only needed for heart

Front 69

WHY DOES AN ANATOMIC DEFECT IN HEART INITIALLY CAUSE A LEFT TO RIGHT SHUNT?

Back 69

The larger, more muscular, left side of the heart generates the higher pressures required to supply blood to the whole body. The smaller, right side of the heart generates the lower pressure required to circulate blood solely through the lungs. If a large anatomic defect exists between the two sides of the heart, blood will flow from the left side to the right side. This results in high blood flow and pressure traveling through the lungs

Front 70

posterior wall infarction means a _____ coronary artery block

Back 70

R coronary a. block

Front 71

VSD is acyanotic, tardive cyanotic, or cyanotic? Why?

Back 71

TARDIVE cyanotic

*MOST COMMON HEART CONGENITAL DEFECT

b/c left>right shunt eventually becomes R>L shunt, overpowering pulmonic arteries (they thicken)

Front 72

myocardial infarction symptoms 6

Back 72

SUDDEN angina
PROLONGED more than 30-40 min
NOT RELIEVED BY NITRO
assoc. w/ DIAPHORESIS & RESTLESSNESS
May awaken person from sleep
DIABETES MELLITUS = SUDDEN DEATH

Front 73

What condition(s) can be included in Rt - Lt CHD?

Back 73

TETROLOGY OF FALLOT


*Eisenmenger's doesn't begin as left to right but does become so. TOF actually starts R>L which is very bad thing

Front 74

3 tests for MI

Back 74

1. EKG (see lab notes) = NORMAL
vs
2. STRESS TEST (exercise EKG) = abnormal then means ISCHEMIC HEART DISEASE
3. ANGIOGRAM via camera thru femoral artery inject dye

Front 75

MOST COMMON A.S.D.

Back 75

ostium SECuNDUM

Front 76

how to clean up blocked CORONARY artery

Back 76

BLAST THROUGH IT! with coronary artery ANGIOBLASTY

50% recurrence w/in 6 mo.

Front 77

In a left to right shunt, why does oxygen in lungs get reduced (what happens to the lungs that causes them to not take up oxygen)?

Back 77

SCARRING due to back flow of blood into lungs.
Scarred tissue DOES NOT HOLD OXYGEN.

Front 78

how to clean up 4 blocked coronary arteries?

Back 78

CORONARY BYPASS (for more than one blocked artery)

Front 79

VSD can be detected by cardiac auscultation. Classically, a VSD causes a pathognomonic holo- or

Back 79

PANSYSTOLIC MURMUR


*A murmur extending through the entire systolic interval, from the first to the second sound.

Front 80

angioplasty

Back 80

removes block of coronary artery (singular)

Front 81

What is the most common congenital heart lesion and what part is it commonly found in?

Back 81

Ventricular Septal Defect (VSD); Found in the membranous part of the IV septum

Front 82

HTN always refers to

Back 82

LEFT SIDE

~AORTIC NARROWING so HIGH PRESSURE
~LEFT ventricle hypertrophies
~then LV failure = death

Front 83

extra heart sounds that are produced as a result of turbulent blood flow that is sufficient to produce audible noise.

Back 83

murmur

Front 84

PHTN always refers to

Back 84

pulmonary hypertension

Front 85

The reduction in oxygen transfer reduces oxygen saturation in the blood, leading to increased production of red blood cells in an attempt to bring the oxygen saturation up.
EXCESS OF RED BLOOD CELLS is called _____________

Back 85

ERYTHROCYTOSIS

Front 86

BP = _______x ________



*BP searches the sea for oil CORES (BP CORES)

Back 86

cardiac output x resistance


BP = COxRES

Front 87

difference b/w ischemia and infarct?

Back 87

ischemia=less blood

infarct=NO blood

Front 88

PRIMARY hypertension
vs.
SECONDARY hypertension

Back 88

IDIOPATHIC - no reason, NO etiology

secondary HTN as the result of something else, has a cause

Front 89

What is the significance of a small ventricular septal defect?

Back 89

No functional significance if the defect is small

Front 90

idopathic HTN

Back 90

primary (no etiology)

Front 91

Why is EISENMENGER's called cyanosis TARDIVE?

Back 91

Eventually, due to increased resistance, pulmonary pressures may increase sufficiently to cause a reversal of blood flow, so blood begins to travel from the right side of the heart to the left side (opposite fr. initial L>R shunt), and the body is supplied with deoxygenated blood, leading to cyanosis and resultant organ damage.

Front 92

CHRONIC CONGESTIVE FAIL

Back 92

ischemia of many small areas

Front 93

What is the clinical significance of a big ventricular septal defect?

Back 93

PANSYSTOLIC MURMUR & RIGHT VENTRICULAR HYPERTROPHY

(and assoc. signs like:)
Fatigue,
dyspnea on exertion (CARDIAC OUTPUT not enough);
Palpitation d/t arrhythmia;
Repeated Lower respiratory infection in childhood;

Front 94

SUDDEN DEATH

Back 94

sudden death (diabetes)

Front 95

Defect agent of Mitral valve stenosis?

Defect agent of PDA?

Back 95

RheuMatic fever = Mitral (aortic stenosis)

Rubella = PDA (cyanose tardive)

Front 96

What is the Eisenmenger complex?

Back 96

INITIAL VSD can eventually result in thickening of pulmonary aa. and increased pulmonary vascular resistance causing the REVERSAL OF SHUNT TO RIGHT >left.

CYANOSE TARDIVE now forcing deoxygenated blood from right into oxygenated blood of left, whereas before it was oxy into deoxy (not as bad?)

Front 97

syncope

Back 97

fainting

Front 98

What does a patient presenting with Eisenmenger complex usually have?

Back 98

Late onset of cyanosis (tardive cyanosis),

RIGHT ventricular hypertrophy and RSHF

Addn'l complications are infective endocarditis and paradoxical emboli
(same as VSD)

Front 99

What is the most common type of atrial septal defect?

Back 99

Ostium secundum type (90% of all cases); Left to right shunt to cause dilation and hypertrophy of the right atrium and ventricle

Front 100

clinical features Atrial Septal Defect, assuming Eisenmenger's syndrome has occurred?

Back 100

RIGHT VENTRICULAR HYPERTROPHY + PULMONARY HYPERTENSION (left side problem) + EJECTION SYSTOLIC MURMUR

dyspnea on exertion- Palpitation d/t arrhythmia -Repeated LRI in childhood- PHTN -R ventricular hypertrophy -Heart failure -Paradoxical emboli - Bacterial endocarditis

Front 101

LUTEMBACHER syndrome?

Back 101

MITRAL stenosis + OSTEUM SECUNDUM ATRIAL septal defect

A very rare form of angiocardiopathy. Heart disease in which atrial septal defect is combined with mitral stenosis. There is usually marked dilatation and hypertrophy of the right side of the heart. The dilated pulmonary artery not infrequently exceeds the size of the aorta. Predominantly in women; usually seen in young adults but may occur in elderly patient

Front 102

With whom is Patent Ductus Arteriosus common?

Back 102

Premature infants and infants whose mothers were infected with
RUEBELLA VIRUS
early in pregnancy.

Front 103

PATENT DUCTUS ARTERIOSIS:
The ductus arteriosus is a normal fetal blood vessel that closes soon after birth. In a patent ductus arteriosus (PDA) the vessel does not close and remains "patent" resulting in irregular transmission of blood between two of the most important arteries close to the heart, the aorta and the pulmonary artery.

NAME CLINICAL FEATURES OF PDA:

Back 103

A patent ductus arteriosus allows a portion of the oxygenated blood from the left heart to flow back to the lungs by flowing from the aorta (which has higher pressure) to the pulmonary artery. If this shunt is substantial, the neonate becomes short of breath: the additional fluid returning to the lungs increases lung pressure to the point that the neonate has greater difficulty inflating the lungs. This uses more calories than normal and often interferes with feeding in infancy. This condition, as a constellation of findings, is called congestive heart failure.

LEFT HYPERTROPHY & FAIL + PUMONARY HYPERTENSION + ENDOCARDITIS
**CONTINUOUS MACHINERY MURMUR**

mumur during both systole & diastole

Front 104

(TOF) is a congenital heart defect which is classically understood to involve four (TETRA)anatomical abnormalities (although only three of them are always present). It is the most common cyanotic heart defect, and the most common cause of blue baby syndrome.

Back 104

overriding aorta

pulmonic ARTERY stenosis

VSD


right ventricular hypertrophy (due to R>L shunt)

*polycythemia may develop as body tries to get more oxygen carriers

Front 105

What are clinical features of Tetrology of Fallot?

Back 105

CYANOSIS "BLUE BABY SYNDROME" - DYSPNEA not enough oxygen - ENDOCARDITIS due to v.s.d.- BRAIN THROMBUS & ABCESS

Surgical correction needed w/in 1st 2 years
Retarded physical dev.

Front 106

What is transposition of the great arteries?

Back 106

AORTA swaps to LEFT VENTRICLE (deoxygenated! - oh shit!)
PULMONARY ARTERY swaps to RIGHT VENTRICLE

Front 107

Who commonly will present with transposition of the great arteries?

Back 107

Males Offspring of diabetic mothers

Front 108

When is Transposition of the great arteries not fatal?

Back 108

If there is an ASD or VSD or PDA

Front 109

What is Coarctation of the aorta?

Back 109

A local constriction immediately below the origin of the left subclavian a. at the site of the ductus arteriosus.

Front 110

COARCTATION of the aorta?

In PDA, the ductus arteriosis doesn't close. In coarctation, there is a narrowing of the AORTA where the ductus arteriosis inserts from the pulmonary artery. If you SQUEEZE THE AORTA, what happens above? Below?

Back 110

Squeeze the aorta in half divides the pressure, too. More above, less below...

HYPERtension ABOVE = nosebleeds, LEFT ventricular hypertrophy, HA, dizziness
HypOtension BELOW = claudication in legs, pallor, weakness

Difference between RADIAL & FEMORAL PULSES

VASCULAR BRUIT

SIGN OF 3 (indentation makes aorta appear as the number '3') & RIB NOTCHING due to enlarged size of vessels on x-rays

Front 111

3 types of AORTIC Stenosis?

Back 111

Congenital (2 semilunars instead of 3 -shows up in not-so-congenial 40's and 50's)

Senile (calcifications in 60's and 70's)

RheuMAtic (rheuMA M + A) = MAMA

Front 112

CONGENITAL STENOSIS presentation and when do symptoms appear?

Back 112

2 SEMILUNAR CUSPS in children INSTEAD OF 3

40''s and 50's decades not so congenial after all!

Front 113

SENILE CALCIFIC AS present and when do symptoms appear?

DIFFERENCE B/W SENILE AND CONGENITAL AS?

Back 113

DEGENERATION over time of AORTIC VALVE itself - CALCIFICATIONS form on leaflets

60's and 70's go SENILE

**congenital aortic stenosis means the there are only TWO leaflets for the aortic valve, instead of usual 3 and this shows up in 40-50 yr olds

Front 114

rheuM/Atic atrial stenosis =

Back 114

rheuM/Atic = Mitral valve stenosis + Aortic valve stenosis

rheuMA = M + A

Front 115

What are clinical features of AORTIC STENOSIS? (4)


LASSt

Back 115

LASSt:

Left sided heart fail - too much pressure, hypertrophy

Angina - pain due to pressure

Syncope - lack of cerebral perfusion (blocked atrium)

Slow S-two (S2) - takes a lot more pressure to open the aortic valve

Front 116

a condition when the lungs cause the heart to fail

Back 116

cor pulmonale

Front 117

What is Endocardial FibroeLEFTosis?

[ELASTOSIS]

Back 117

Fibroelastic thickening of the endocardium of the LEFT VENTRICLE

which can also affect the valves. Valves may show collagenous thickening. Papillary mm. and chordae tendinae are thick and short. Dev. progressive heart failure.

Front 118

an increase in blood pressure in the pulmonary arteries, vein or capillaries causing fainting (syncope), shortness of breath (dyspnea on exertion), angina, peripheral edema and hemoptysis.

Back 118

pulmonary hypertension

Front 119

What is Dextrocardia?

Back 119

Rightward orientation of the base-apex axis of the heart. Assoc. w/ a mirror image of the normal left-sided location and config. If situs inversus heart functions normal.

Front 120

Pulmonary _________ hypertension typically presents with shortness of breath while lying flat or sleeping (orthopnea or paroxysmal nocturnal dyspnea), while pulmonary _______hypertension (P_H) typically does not.

*think: which one carries OXYGENATED blood to the heart for pumping into the system?

Back 120

VENOUS!

Pulmonary vein carries oxygen to left ventricle = NO OXYGEN, NO BREATH
Pulmonary VEIN hypertension = DYSPNEA


pulmonary artery carries deoxy so typically no shortness of breath

Front 121

What is ISCHEMIC heart disease and when does it develop?

Back 121

CORONARY ARTERY ATHEROSCLEROSIS;

when blood flow is TOO LOW to meet the O2 demands of the heart.

Front 122

When there is lung disease present, like emphysema, chronic obstructive lung disease (COPD) or pulmonary hypertension- the small blood vessels become very stiff and rigid. The right ventricle is no longer able to push blood into the lungs and eventually fails. This is known as pulmonary heart disease. Pulmonary heart disease is also known

Back 122

RSHF or Cor Pulmonale

Front 123

What is the leading cause of death and what are the 4 SYNDROMES?

I-[MACS]

Back 123

ISCHEMIC HEART DISEASE (80% of deaths);

I-MACS:
Ischemia -
Myocardial infarct,
Angina pectoris,
CHF,
Sudden death

Front 124

The chief cause of right heart failure is the increase in blood pressure in the lungs (pulmonary ______).

Back 124

artery

Front 125

Blood backs up into the systemic venous system, including the hepatic vein. Chronic congestion in the centrilobular region of the liver leads to hypoxia and fatty changes of more peripheral hepatocytes, leading to what is known as nutmeg liver.

Back 125

cor pulmonale (wiki calls it pulmonary heart disease)

Front 126

INFARCTION

Back 126

a part of the heart is dead due to loss of blood supply

Front 127

ANGINA PECTORIS

Back 127

chest pain

Front 128

make card based on renal

Back 128

htn story in notes

Front 129

UNSTABLE ANGINA

Back 129

PRE-INFARCTION= no work but EVEN AT REST, BLOOD SUPPLY IS NOT ENOUGH

PAIN @ REST

Front 130

STABLE ANGINA heart condition means

Back 130

ENOUGH cardiac output for normal things but ANGINA PECTORIS during EXERCISE that goes away during REST

REST = GOES AWAY
Need a vasodilator

Front 131

LSHF causes __________ of the heart

Back 131

hypertrophy of the Left ventricle

Front 132

other word for unstable angina

Back 132

PRE-INFARCTION angina

Front 133

retention of urine _______ blood pressure

Back 133

increases

Overloads the system!

Front 134

What is ANGINA PECTORIS and when does it become symptomatic?

Back 134

CAD becomes symptomatic only when the LUMEN cross sectional area of affected vessel is REDUCED by more than 75%.

Use VASODILATOR = sublingual nitroglycerin (dilates the coronary arteries, more blood to heart)

Substernal pain radiating to the L arm, jaw and epigastrium;

Front 135

What brings on chest pain, what is the duration and how is it relieved?

Back 135

recurrent episodes usually brought on by increased physical activity or emotional excitement; 1-15 min.; reducing physical activity or sublingual nitroglycerin (vasodilator).

Front 136

arterial stenosis __________ blood pressure

Back 136

increases

Stepping on the hose makes the opening smaller and pressure higher with volume lower

Front 137

What are other causes of angina and what is an atypical cause?

SEE INDIVIDUAL CARDS FOR EACH

Back 137

Coronary vasospasm, AS, or aortic insufficiency; Prinzmetal angina (variant angina) occurs at rest and caused by coronary a. spasm occurs in structurally normal coronary aa.

Front 138

LSHF causes ____ lungs

Back 138

wet

Front 139

hypoKalemia and hypertension

Back 139

CONN'S SYNDROME :
(big Al Dosterone from the zona glomerulus goes to distal tubule and grabs salty girls, kicks out potassium bums)

increased sodium (hyperNatremia)and decreased K+ (hypoKalemia)/potassium

Front 140

What is UNSTABLE angina?

Back 140

PREinfarction angina, assoc. w/ dev. of nonocclusive thrombi over atherosclerotic plaques.

accelerated angina or crescendo angina; pain at work AND rest and sublingual nitroglycerin won't work; NOT RELATED TO EXERCISE OR REST, may occur during rest or sleep

Front 141

hyperKalemia

Back 141

high K+ alemia (blood)

Front 142

LSHF causes these changes in the kidney (4)

Back 142

decreased SIZE
decreased PERFUSION of nutrients
decreased URINE PRODUCTION
decreased BLOOD SUPPLY

Front 143

hyperNA+tremia

Back 143

high Na+ emia (blood)

Front 144

UNSTABLE ANGINA presentation and progression

Back 144

NORMAL EKG
NO CARDIAC ENZYMES elevated or present

w/o pharmacologic or mechanical intervention to "open up" coronary narrowing many pt.s progress to MI

Front 145

an alteration in structure of RIGHT ventricle (R. ventricular hypertrophy and dilation) and fcn of right ventricle SECONDARY to PULMONARY hypertension

Back 145

COR PULMONALE

acute c.p.. = massive pulm embolism and ARDS
chronic c.p. = COPD, pulmonary fibrosis and kyphoscoliosis

Front 146

LSHF causes inadequate ________ in the brain

Back 146

perfusion of nutrients/blood supply

Front 147

In cor pulmonare, the ventricles are equally _________.

Back 147

THICK (chronic)

Intraventricular septum LOSES CURVATURE TOWARDS LEFT and becomes straight

Front 148

How does an MI look on tests?

Back 148

Positive EKG and cardiac enzymes present in blood.

Front 149

What kind of symptoms are seen w/ cor pumonale?

Back 149

RVF (pitting edema, pumonary hypertension, hepatomegaly, tender liver, peripheral pitting edema, splenomegaly, ascites)

Front 150

LSHF causes these changes in the muscle:

Back 150

decreased PERFUSION (nutrients via blood supply) so FATIGUE & WEAKNESS

Front 151

If pateint has both MITRAL valve stenosis and AORTIC valve stenosis, then he had ____________ as a child.

Back 151

RHEUMATIC FEVER

Front 152

What are complications of MI? (7)

Back 152

1. CHRONIC CHF -heart is scarred, fibrosed and pumps less efficiently so less blood gets out
2. Sudden death d/t VENTRICULAR FIBRILLATION - necrotic myocytes interrupt intercalated disc synchoronicity or scarred tissue doesn't conduct electricity as well?
3. RUPTURE - cardiac TAMPONADE - HEMOPERICARDIUM: All the way through endo-myo-pericardium as transmural rupture spills blood into pericardium and fluid builds up quickly around heart, squeezing it to death.
4. VENTRICULAR ANEURYSM -Tear in a thinned, weak wall. Just a big fucking tear that kills you
5. MURAL THROMBUS & EMBOLISM - clot gathers (thrombus) in coronary artery or subendocardium, or clot ruptures and breaks free (embolus), blocking a major coronary artery
6. PERICARDITIS- inflammation/pus/edema around heart due to sick pericardium
7. POSTMYOCARDIAL INFARCTION SYNDROME (Dressler syndrome) - the Dr. Chris Dressler syndrome, a friend of mine in chiro school whose name I'm using to remember this MI complication

Front 153

In mitral stenosis (ie, from rheumatic fever), what happens to the CARDIAC OUTPUT?

Back 153

drops so DYSPNEA on EXERTION

Front 154

ANYTHING TO DO WITH THE KIDNEY IS GOING TO ______ THE BLOOD PRESSURE

Back 154

INCREASE

Front 155

With mitral stenosis, what happens to LEFT ATRIuM?

Back 155

gets larger due to increased pressure

Front 156

What is pericarditis?

Back 156

Transmural MI involves epicardium -> inflam of pericardium; manifested as chest pain and may produce a pericardial friction rub. 1/4 w/ acute MI dev. pericardial effusion.

Front 157

What is Dressler syndrome?

Back 157

Post MI syndrome; delayed form of pericarditis that dev. 2-10 weeks after infarct. Antibodies to heart m. appear in these pt.s corticosteroids improve...may be immunologic.

Front 158

Mitral stenosis, causes ________ heart failure even thought it doesn't enlarge.

Back 158

left ventricle

Front 159

What conditions influence the supply of blood to the heart?

Back 159

Atherosclerosis and thrombosis of the ruptured ATHEROMA
Thromboemboli LOOSE EMBOLUS TO LUNG OR HEART OR BRAIN
Coronary artery spasm FIBRILLATION
High BP HYPERTENSION increases pulmonic load stenoses of valves hypertrophy kidney decrease in size fcn and output and decreased oxygen to all organs so wet lungs and cerebral ischemia

, Cardiac Output reduction and low heart rate

due to turbulence or increased pressure tears intima of aorta and creates false tunnel for blood Dissecting aneurysm

Front 160

Since left atrium enlarges but left ventricle does not, the right ventricle becomes HYPERTROPHIED. Increased pulmonary pressure. History indicates

Back 160

mitral valve stenosis due to RHEUMATIC FEVER as a child

Front 161

What conditions influence the availability of oxygen in the blood?

Back 161

ANEMIA - CARBON MONOXIDE - CYANIDE

Front 162

clinical syndrome of HYPOTENSION, peripheral VASOCONSTRICTION, OLIGURIA (low urine output) and often impairment of CONSCIOUSNESS

Back 162

ACUTE CIRCULATORY FAILURE

Front 163

What conditions increase oxygen demand/increase cardiac work?

Back 163

HTN Valvular stenosis or insufficiency Hyperthyroidism Fever Thiamine deficiency Catecholamines

Front 164

etiology of ACUTE CIRCULATORY FAILURE

Back 164

Inadequate cardiac output due to:
Bleed out/Cardiac generated/blood Poisoning

1. HYPOVOLEMIC shock (eg, hemorrhage)

2. CARDIOGENIC shock (eg. acute myocardial infarction & acute massive pulmonary embolism)

3. SEPTIC shock

Front 165

What are the 3 locations of infarction?

Back 165

Posterior - inferior infarction

Anterior - wall infarction

Lateral - wall infarction

Front 166

3 types of SHOCK that cause acute circulatory failure:

Back 166

1. HYPOVOLEMIC (hemorrhage)
2. CARDIOGENIC (MI & lung embolism)
3. SEPTIC

Front 167

What is a subendocardial infarct?

Back 167

Affects the inner 1/3 to 1/2 of the LV

Front 168

Complications of SHOCK (hypovolemic due to blood loss, cardiogenic due to heart attack or pulmonary embolism, septic shock due to toxin) if NOT HANDLED IMMEDIATELY`

Back 168

KIDNEY FAILURE (heart fail always causes kidney fail)

HYPERKALEMIA (too much K+)

LETHAL CARDIAC ARREST

BRAIN DAMAGE permanent (no O2)

Front 169

What is LAD coronary artery infarct?

Back 169

Occlusion of this a. results in apical, anterior and anteroseptal walls of the left ventrical (anterior infarct)

Front 170

Clinical signs of acute circulatory failure (shock) due to hypovolemic, cardiogenic, or septic...

Back 170

Skin is blue (cyanosis)
BP low (blood loss, incompetence of heart, no O2)
Heart rate crashes
Oliguria (low urine output)
Confused mental status

Front 171

What type of infarct results in the L circumflex coronary a.?

Back 171

Occlusion results in a LATERAL infarct.

Front 172

How does MI develop?

Back 172

SUBENDOCARDIUM affected first, then takes several hours for signs

Front 173

What occurs with TRANSIENT coronary occlusion?

Back 173

May cause only SUBENDOCARDIAL necrosis,

persistent occlusion -> TRANS-MURAL necrosis.

Thrombolytic drugs interrupt and limit myocardial necrosis

Front 174

INFARCTS are usually LEFT VENTRICLE. Why?

Back 174

WORKLOAD elevated compared to smaller right side that only needs pumping power to pulmonary artery

Front 175

What is seen with gross examination of acute MI?

Back 175

24 hours pallor noticed 3-5 days: mottled and sharply outlined, w/ necrotic region bordered by hyperemic zone. 2-3 weeks: region depressed and soft w/ refractile, gelatinous appearance. Older are firm and have pale, gray appearance of scar tissue

Front 176

What is Reperfusion of Ischemic Myocardium?

Back 176

Contraction band necrosis: contraction bands thick, irregular, transverse eosinophilic bands in neccrotic myocytes. Typically hemorrhagic d/t blood flow through damaged microvasculature.

Front 177

What is HTN? ******memorize

Back 177

A persistent increase of systemic BP above 120 mm systolic or 80 mm diastolic or both.


116/76 is normal but anything beyond is prehypertensive

Front 178

What is considered normal BP and prehypertension?

Back 178

Normal: = 116/76 mm Hg

PreHTN: >116/76,

HIGH < 120/80 mm Hg

Front 179

What is the most prevalent and serious cause of ISCHEMIC HD (& MYOCARDIAL INFARCT) in the U.S. and what are the stages?

Back 179

HYPERTENSION!!!!

Stage 1= 140/90

Stage 2 >160/100;

Stage 3: >180/110

Front 180

What does chronic HTN lead to?

Back 180

Pressure overload resulting first in compensatory LEFT VENTRICULAR HYPERTROPHY and eventually cardiac failure.

Front 181

When is the term hypertensive heart disease used?

Back 181

Heart is enlarged in the absence of a cause other than HTN. (cardiomegaly)

Front 182

What does HTN cause?

Back 182

LEFT VENTRICULAR CONCENTRIC HYPERTROPHY due to increased cardiac workload.
Weight increases.

Front 183

What is BP the product of?

Back 183

CO X PR CO increases d/t high blood volume, high Na content and increased HR; PR raises d/t vasoconstriction.

Front 184

What are the types of HTN?

Back 184

Primary or essential Secondary

Front 185

What is Primary HTN?

Back 185

95% of HTN >45 y/o
Unknown etiology IDIOPATHIC

Insidious onset until target organs are involved.
More common in balcks, male, familial Hx, smoking stress and obesity.

Front 186

What are the end organs/target organs in PRIMARY HTN?

Back 186

Heart
Kidney
Brain
Eyes

Front 187

What are clinical symptoms and nonspecific signs of PRIMARY HTN?

Back 187

asymptomatic and black, male, over 45

in some pounding morning HA;

LEFT VENTRICULAR HYPERTROPHY,

SHIFTED APICAL IMPULSE (cardiomegaly) and S4 SOUND

Front 188

SECONDARY HTN

who?
why?

Back 188

HAPPENS TO THE YOUNG Pt <35 y/o, FACIAL EDEMA, ACROMEGALY

secondary to something else: KIDNEY dz, ADRENALS (Cushings and Conns), PITUITARY TUMOR, COARCTATION (squeezing of aorta), preeclampsia (TOXEMIA), THYROID HYPER

Front 189

How do the specific etiologies of SECONDARY HTN commonly present?

Back 189

KIDNEYdz: facial edema FLUID RETAINED

Adrenal cortex: as CONN'S= HYPER-Na-TREMIA, HYPO-K-ALEMIA and ALdosterone in plasma

Adrenal medulla: CUSHINGS= high CATECHOLAMINES in plasma and urine

Pituitary: ACROMEGALY

PRE-ECLAMPSIA - pregnant TOXEMIA

Thyroid: hyperthyroidism GRAVES exophthalmos

Front 190

What are renal causes of secondary HTN?

Back 190

1. POLYCYSTIC kidney
2. RENIN- secreting tumor
3. Renal ARTERIAL. stenosis
5. Chronic GLOMERULONEPHRITIS

Front 191

What are ADRENAL causes of secondary HTN? (3)

two men's names and a pheo

Back 191

PHEOCHROMOCYTOMA = hypertension due to tumor in medulla that secretes E & NE (epinephrine and norepinephrine) all the time

CONN'S = Big Al Dosterone visits the kidney distal tubule from his bachelor pad in the zona glomerula of the adrenal cortex. He grabs all the salty girls and kicks the potassium bums to the street, only he does it too much to show off and now there is HYPERNATREMIA nd HYPOKALEMIA

CUSHING'S = too much damn CORTISOL! Tiger in the room all the time! Blood test for glucocorticoid/glucose.

Front 192

What are complications of PRIMARY & SECONDARY HTN?

Back 192

DIASTOLIC dysfxn (MOST COMMON) can lead to CHF due to LEFT VENTRICULAR FAILURE

LVHypertrophy (orthopnea, dyspnea) = failure -increased O2 demand-LEADS TO MYOCARDIAL INFARCT b/c less blood supply so hypertensive means heart attack comin' 80% of time

INTRACEREBRAL hemorrhage RUPTURED BERRY ANEURYSM of cerebral circulation lenticular stria artery-STROKE

DISSECTING aneurysm of aorta (sudden death)

RENAL failure d/t NEPHROSCEROSIS if HTN severe (25% blood of heart goes to kidney so hypertension causes heart THEN kidney failure)

Eye: RETINAL ARTERies constrict in response to HTN (COPPER WIRE ARTERIOLES)

Increased blood pressure causes renal artery LEAK leaving HARD EXUDATE

Front 193

COR PULMONALE presentation

(cor pulmonale is lungs crash heart)

Back 193

1. PHTN (cor pulmonale is lungs crash heart)

2. RIGHT VENTRICULAR HYPERTROPHY and DILATION

*pulmonary artery/pulmonary venous pressure increased so blowing hard into ventricle. Ventricle expands and hypertrophies to take the increase.

Front 194

What is acute cor pulmonale?

Back 194

sudden massive PULMONARY EMBOLISM & ACUTE/ADULT RESPIRATORY DISTRESS SYNDROME

all sx of RSHF

Front 195

What is cardiac TAMPONADE?

stick a tampon in a water bottle and it plugs it up- better use a Beck's bottle

Back 195

A syndrome - RAPID ACCUMULATION of FLUID that restricts the VENOUS filling.

x-ray: has a WATER BOTTLE APPEARANCE

Life threatening. BECK'S TRIAD: HyPOtension, Increased JVP, muffled heart sounds also assoc. with PERICARDITIS

Front 196

causes of chronic COR PULMONALE (3)

what happens to the RIGHT VENTRICLE and what is result?

Back 196

COPD - PULMONARY FIBROSIS - KYPHOSCOLIOSIS

*Pulmonary fibrosis is suggested by a history of progressive shortness of breath (dyspnea) with exertion. Sometimes fine inspiratory crackles can be heard at the lung bases on auscultation
\.
Cor pulmonale is the lung killing the heart. The right ventricle thickens and this straightens out the IVS curve, which is normally apex to the left. Flattening out the left ventricle. Symptoms are RSHF with pulmonary symptoms

Front 197

What is rheumatic heart disease?

Back 197

d/t acute rheumatic fever; untreated pharyngitis

A & B hemolytic streptococcus. B

produce antistrept. antibodies that w/ T cells react w/ cardiac antigens & may involve patho. effects on layers of heart.
BACTERIAL ENDOCARDITIS
JONES' MAJOR CRITERIA (carditis, chorea, erythema marginatum, or subcutaneous nodules)
JONES' MINOR CRITERIA (arthralgia, fever, EEL =EKG, ESR, Leukocytosis)

Front 198

ACUTE rheumatic heart disease causes what OVERALL condition?

Back 198

PANCARDITIS

endo, myo, peri levels all affected

Front 199

What is rheumatic fever?

Back 199

A multisystem childhood disease that follows a strept. infection involving heart, joints, CNS and skin.

Front 200

How does MYOCARDITIS histopath present?

Back 200

ASCHOFF BODY is granulomatous lesion
OWL-EYE AND CATERPILLAR APPEARANCE

ANITSCHOW cells unusual cells in ASCHOFF body whose nuclei have a band of CHROMATIN. May become multinucleated termed Aschoff giant cells.

Front 201

PERICARDITIS presentation

Back 201

FIBRIN CRYSTALS = BREAD & BUTTER with CHEST PAIN + FRICTION RUB

It can be caused by a variety of causes including viral infections of the pericardium, idiopathic causes, uremic pericarditis, bacterial infections of the precardium (for i.e. Mycobacterium tuberculosis), post-infarct pericarditis (pericarditis due to heart attack), or Dressler's pericarditis.

The classic sign of pericarditis is a friction rub auscultated on the cardiovascular examination usually on the lower left sternal border.[2] Other physical signs include a patient in distress, positional chest pain, diaphoresis (excessive sweating), and possibility of heart failure in form of precardial tamponade causing pulsus paradoxus, and the Beck's triad of hypotension (due to decreased cardiac output), distant (muffled) heart sounds, and JVD (jugular vein distention).

Front 202

How does endocarditis present? MOST IMPORTANT W/ RHEUMATIC FEVER

Back 202

VALVE Dz: Heart valves become inflamed and present fibrin NODULES called "VERRUCAE"

MITRAL valve (1st affected) and AORTIC valve (2nd) most affected than right sided valves. SO ALL LEFT SIDED HEART FAIL

Front 203

What is required in Jone's criteria to DIAGNOSE RHEUMATIC heart disease?

Back 203

Dx of RHD based on Jone's criteria: 2 major or 1 major and 2 minor clinical manifestations.

Front 204

What are major manifestations in JONE'S criteria

(1 MAJOR AND 2 MINOR OR 2 MAJOR clinical manifestations required for rheumatic diagnosis)

Back 204

CARDITIS: murmurs, cardiomegaly, pericarditis and CHF;

JOINTS: migrating or fleeting POLYARTHRITIS (child cannot play - joints affected migrating)

NEUROSYSTEM: chorea = sentinal system so writhing body movements

SKIN: erythema marginatum (redness/rashes), subcutaneous nodules under skin.

Front 205

What are minor (NON-SPECIFIC) manifestations in Jone's criteria?

Back 205

Arthralgia
Fever Raised FEBRILE
ESR =EOSINOPHILIC. SEDIMENTATION RATE
Leukocytosis = LOW LEUKOCYTES
Positive C reactive protein
EKG changes

Front 206

What are complications of Chronic Rheumatic Heart Disease?

WHAT IS MOST IMPORTANT COMPLICATION?

Back 206

1. Bacterial endocarditis follows bacteremia SO NEED PROPHYLATIC ANTIBIOTICS

2. MURAL thrombi = wall
3. Congestive cardiac failure
4. Adhesive pericarditis
5.******* MITRAL stenosis then AORTIC stenosis or mitral valve PROLAPSE******

Front 207

What causes MITRAL Stenosis?

Back 207

RHEUMATIC FEVER!

Chronic RHEUMATIC H.D. -> formation of fibrous ADHESIONS b/w leaflets of MITRAL VALVE and "FISH-MOUTHED" mitral stenosis

Front 208

What are some s/s of MITRAL stenosis? (from rheumatic)

Back 208

decreased CO,
increased LA pressure,
LVF then RVF; *****COMBINATION OF BOTH SIDED FAILURE****
Emboli:
LA enlargement-fibrillation=presses on LEFT RECURRENT. LARYNGEALn.-HOARSENESS of voice

Front 209

What is always associated w/ mitral stenosis?

Back 209

Aortic stenosis (rheumatic AS)

Front 210

What is Mitral Valve PROLAPSE?

Back 210

PROLAPSE OF ONE OR BOTH LEAFLETS INTO THE ATRIUM W/ BALLOON-SHAPHED APPEARANCE INSTEAD OF SCALLOPED MARGINS

~LEAFLETS become enlarged, redundant,

~CHORDAE TENDINAE become thinned,elongated and billowed

~LEAFLETS PROLAPSE into the LEFT atrium during SYSTOLE

Front 211

What are risk factors of mitral valve prolapse?

MEMORIZE THE 4

Back 211

FAMILIAL(#1),
MARFAN'S
HYPERTHYROIDISM
RHEUMATIC FEVER

Front 212

What are clinical features of mitral valve prolapse?

Back 212

ASYMPTOMATIC in most pt.s,

SYSTOLIC murmur (palpitation sx),

ATYPICAL chest pain IS UNPREDICTABLE

Front 213

What are complications of mitral valve prolapse?

Back 213

Mitral REGURGITATION (and incompetence)

INFECTIVE ENDOCARDITIS caused by ANY abnormal valve

Front 214

What is bacterial endocarditis?

Back 214

INFLAMMATION of cardiac VALVES by bacteria.

Can be classified as acute or subacute bacterial endocarditis.

Front 215

What are the clinical features of bacterial endocarditis?

Back 215

Fever (1st) New murmurs or changing murmurs Positive blood cultures

Front 216

What can occur with infective thromboemboli?

Back 216

Emboli break up and lodge in small vessels, CNS: subarachnoid hemorrhage, CVS: acute congestive failure, Kidney: hematuria, Eye: Roth's spots, Nails: splinter hemorrhage.

Front 217

What is Acute Bacterial Endocarditis?

Back 217

Infection of a normal cardiac valve by a highly virulent suppurative organisms (s. aureus and pyogenes)

Front 218

What is Subacute Bacterial Endocarditis?

Back 218

Less virulent organisms affecting a structurally abnormal valve (MS, MVP)

Front 219

What are risk factors for BACTERIAL ENDOCARDITIS?

Back 219

1. RIGHT HD:Mitral valve:aortic valve (4:1)

2. IV drug abusers SHOOT RIGHT (while RhuMatic is LSHF)

3. Prosthetic valves

4. children with congenital heart disease

Front 220

What is myocarditis?

Back 220

Inflam. of the myocardium associated w/ myocyte necrosis and m. degeneration.

Front 221

What are primary and secondary myocarditis d/t?

Back 221

!. infectious etiology, either viral or protozoal

2. Rheumatic fever (SYSTEMIC LUPUS ERYTHEMA, TB, sarcoidosis)

Front 222

What is viral MYOCARDITIS, what causes it and what are sx?

EKG, FEVER, CHEST PAIN HALLMARKS

Back 222

VIRAL MYOCARDITIS: due to organisms or protozoa. MOST COMMON = VIRAL

Acute myocarditis; coxsachie and rubella viruses; asymptomatic but lead to debilitating loss of cardiac function mainly in children or YOUNG adult.

Front 223

Describe hyperthyroidism.

Back 223

Causes increased HR (tachycardia) Increased workload & CO eventually leads to high output failure.

Front 224

Describe hypothyroidism.

Back 224

Opposite hyper- Decreased HR (bradycardia) Impaired myocardial contractility Decreased CO Heart is flabby and dilated b/c of myxedema

Front 225

What is Deficiency: Wet Beriberi?

Back 225

ALCOHOLICS or B12 (COBALAMIN) deficient people

Peripheral vasodilation - high CO - salt water retention - pedal edema - increased cardiac workload - tachycardia - edema - increased a. & v. pressure All lead to myocardial injury expressed as chest pain.

Front 226

What are 3 metabolic diseases of the heart?

Back 226

1. Hyperthyroidism 2. Hypothyroidism 3. Thiamine deficiency: Wet Beriberi

Front 227

What is cardiomyopathy and the 5 types?

Back 227

NONinflammatory disorder of myocardium NO INFLAMMATION & MUSSLCES ARE NOT DYING

1. Idiopathic dilated cardiomyopathy
2. Toxic cardiomyopathy
3. Cardiomyopathy of pregnancy
4. Hypertrophic cardiomyopathy
5. Restrictive cardiomyopathy

Front 228

What is the most common type of cardiomyopathy, what occurs and the etiology?

Back 228

Idiopathic dilated cardiomyopathy Symmetrical hypertrophy and biventricular dilatation, decreased contractile force of L & R ventricle -> CHF Et: mostly idiopathic, may be d/t alcohol, doxarubicin and thiamine deficiency (75% end up w/ CHF w/in 5 yrs)

Front 229

What causes toxic cardiomyopathy?

Back 229

Alcohol: ethanol has an immediate negative inotropic effect on the heart.

Front 230

When does cardiomyopathy of pregnancy develop, who is commonly affected and what is the result?

Back 230

Last trimester or 1st 6 mos after delivery MC in black race and multiparous women, some have spontaneous recovery rest end up w/ CHF.

Front 231

What is hypertrophic cardiomyopathy also known as, how is it inherited and what part of the heart does it affect?

Back 231

Idiopathic hypertrophic subaortic stenosis Autosomal dominant type; no dilatation but asymmetrical hypertrophy (IV septum) that affects LV mostly.

Front 232

What are clinical features of Hypertrophic cardiomyopathy?

Back 232

Apparent when pt young adult male. angina, atrial fibrillation, may result in sudden death.

Front 233

What is restrictive cardiomyopathy?

Back 233

A group of diseases (sarcoidosis, hemochromatosis & amyloidosis) where contractile function of heart remains normal but limits diastolic filling.

Front 234

What are 4 causes of sudden cardiac death?

Back 234

1. Coronary artery disease (MI) 2. Aortic stenosis 3. Hypertrophic cardiomyopathy 4. Ventricular fibrillation

Front 235

What are 3 types of cardiac tumors?

Back 235

1. Cardiac myxoma 2. Rhabdomyoma 3. Metastatic tumor

Front 236

What 2 cardiac tumors are benign and what are they?

Back 236

Cardiac Myxoma: 75% arise in LA as glistening gelatinous 5-6cm polypoid mass w/ a stalk; may obstruct mitral orifice. Rhabdomyoma: **MOST COMMON***; in infants & children; nodular masses in myocardium.

Front 237

Where do metastatic tumors of the heart usually originate?

Back 237

Lung, breast and malignant melanoma.

Front 238

What is acute pericarditis?

Back 238

Inflammation of pericardium

Front 239

What are symptoms of acute pericarditis, what relieves and aggravates it?

Back 239

sudden, sharp, substernal chest pain that may refer to the neck or shoulder and relieved by sitting forward.

**AGGRAVATED BY LYING DOWN/MOVEMENT/RESPIRATION
***RELIEVED BY LEANING FORWARD

Front 240

What is pericardial effusion?

Back 240

Accumulation of excess fluid in the pericardial cavity in the form of transudate or exudates

Front 241

What can serous pericarditis be d/t?

Back 241

CHF

Front 242

What can chylous pericarditis be d/t?

Back 242

lymph exudate; could be from lymphoma

Front 243

What can hemopericarditis be d/t?

Back 243

metastatic CA

Front 244

What is cardiac tamponade and Beck's triad?

Back 244

Rushing of blood into pericardial cavity that restricts the venous filling; hypotension, increased JVP and muffled heart sounds

Front 245

What is constrictive pericarditis?

Back 245

Chronic fibrosing disease evolved from TB or radiation therapy to mediastinum, pericardial cavity is obliterated. It compresses the heart and restricts blood flow.

Front 246

What are pulmonary sequestrations?

Back 246

a portion of the lower lobe of lung receives blood supply from aorta but w/ no connection to rest of lung.

Front 247

What is tracheoesophageal fistula?

Back 247

Communication b/w part of the esophagus and trachea can lead to aspiration pneumonia.

Front 248

What is the result of Alfa1 antitrysin deficiency?

Back 248

emphysema

Front 249

What is Allergic rhinitis? Hay fever, although no hay, no fever.

Back 249

Type 1 hypersensitivity reaction (dermatitis, food poisoning, allergic rhinitis)

etiology can be pollen;

nasal irritation, sneezing, watery rhinorrhea (running eyes), itchy eyes, soft palate and ears. all at once due to TRIGEMINAL NERVE

Front 250

What can cause laryngeal obstruction?

Back 250

Allergic edema, inhaled foreign body, inhaled vomitus, tumors of larynx.

Front 251

What are tumors of the larynx?

Back 251

Squamous cell carcinoma; associated w/ tobacco (cigar) and alcohol use

Front 252

What is pulmonary hypertension, where is it seen and what does it lead to?

Back 252

Increase in thickness of tunica media resulting in increased pressure in pulm. aa. seen in lt-rt shunt or MS or COPD; leads to respiratory failure.

Front 253

What are clinical features of a pulmonary embolism?

Back 253

Dyspnea, sudden chest pain d/t lung infarction, hemoptysis

Front 254

What are risk factors for acute bronchitis?

Back 254

air pollutants, allergies, chronic sinusitis, exposure to chemicals, fumes, dust and smoke inhalation.

Front 255

What are s/s of acute bronchitis?

Back 255

persistent dry cough, then sputum prod'n, malaise, low-grade fever, insomnia, sx last 3-7 days and dry cough persists several weeks.

Front 256

What is atelectasis?

Back 256

incomplete expansion of lung or collapse of already expanded lung; 2 types: acquired and congenital

Front 257

Discuss Acute respiratory distress syndrome (ARDS).

Back 257

Sudden, life threatening lung failure, an acute diffuse alveolar damage; injury to alveoli or capillaries inflame the alveoli causing them to fill w/ liquid and collapse; gas exchange ceases; mechanical ventilation is tx.

Front 258

What are causes of ARDS?

Back 258

1. Serious infection of blood or other tissues (sepsis) 2. Severe lung infection 3. inhalation of smoke or other toxic fumes 4. Near drowning

Front 259

What are s/s of ARDS and how is it diagnosed?

Back 259

Dyspnea, tachypnea, severe hypoxaemia, cyanosis; abnormalities in the arterial blood gas analysis [O2] and [CO2] and pH of blood

Front 260

What is neonatal respiratory distress syndrome and what is evaluated in amniocentesis?

Back 260

Hyaline membrane disease; preterm infants (<34 weeks gestation) immaturity of type II pneumocytes, inadequate surfactant; lecithin and sphyngomyelin ratio measured for lung maturity.

Front 261

What are clinical factors of bacterial pneumonia?

Back 261

Abrupt onset of high fever, malaise and productive cough; lead to lung abscess and brain abscess

Front 262

What are clinical features of viral pneumonia?

Back 262

Caused by cytomegalo virus; low grade fever, dry cough, HA and malaise.

Front 263

What is a lung abscess?

Back 263

Localized accumulation of pus with cough, fever and foul-smelling sputum.

Front 264

What can cause a lung abscess? (3)

Back 264

1. Alcoholic: aspiration MC cause 2. Pneumonia 3. Aspiration at dentist's office

Front 265

What is primary TB?

Back 265

Caused by mycobacterium tuberculosis inhalation that replicates in alveoli and leads to form'n of
*****GHON'S FOCUS*****

, Ghon's complex and may become secondary TB (5% of cases)

Front 266

What is Ghon's focus w/ primary TB?

Back 266

PERIPHERAL PARENCHYMAL GRANULOMA in the upper lobes, 1-2cm in diameter w/ a CENTRAL NECROSIS.

Front 267

What is secondary TB?

Back 267

Reactivation of the primary TB or reinfection; mult. granulomas w/ extensive tissue necrosis in any part of lung

Front 268

What can happen with secondary TB?

Back 268

May heal or calcify or may erode into a bronchus & cause a tuberculous cavity w/ caseous necrosis; complications: miliary TB and hemoptysis, can get in blood and then can travel anywhere (e.g. Pott's)

Front 269

What is different w/ TB that is not seen in pulmonary embolism?

Back 269

Fever and organisms in sputum.

Front 270

What is COPD and what is involved?

Back 270

Chronic OBSTRUCTIVE Pulmonary Disease; Tubes are involved w/ "obstructive"

Front 271

What is included in COPD?

Back 271

Chronic bronchitis and Emphysema

Front 272

What characterizes COPD?

Back 272

Decreased forced expiratory volume Decreased air flow either by an increase in resistance w/in the airways or a reduction in the outflow pressure.

Front 273

What causes increased resistance in airways and reduction in outflow pressure?

Back 273

Narrowed airways in chronic bronchitis or asthma; Loss of elastic recoil as in emphysema

Front 274

What is chronic bronchitis?

Back 274

Inflammation of the bronchi w/ persistent productive cough for at least 3 months for 2 successive years.

Front 275

What can cause chronic bronchitis?

Back 275

Tobacco smoke, dust, fumes and pollution

Front 276

What are clinical factors of chronic bronchitis?

Back 276

Begin as winter cough lasts 2 years (steady increase w/ lot of sputum); Wheeze, dyspnea & tightness in chest especially in the am; w/ progression exertional dyspnea, cyanosis &/or cor pulmonale.

Front 277

What is emphysema?

Back 277

Enlargement of the alveoli distal to the terminal bronchioles w/ destruction of the interalveolar septum.

Front 278

What causes emphysema?

Back 278

Alpha1 antitrypsin deficiency and cigarette smoking

Front 279

How does a patient present with emphysema?

Back 279

Prolonged history of exertional dyspnea (low O2) and a minimal non-productive cough.

Front 280

What is asthma?

Back 280

A chronic inflam disorder of the airways that causes recurrent episodes of expiratory wheezing, breathlessness, chest tightness and coughing esp. at night or early am. A cond'n where bronchial tubes in lungs react to different stimuli by becoming inflamed

Front 281

What is recurrent and reversible asthma?

Back 281

Asthma usually associated w/ widespread but variable airflow obstruction that is often reversible

Front 282

What is chronic and lethal asthma?

Back 282

Severe continuing attack of asthma (status asthmaticus) is a serious concern that can lead to respiratory failure and death.

Front 283

What are stimuli/triggers for asthma?

Back 283

exercise, cold air, allergens, infections, emotional reactions and certain medications. Inflammation leads to bronchoconstriction. Type I hypersensitivity reaction.

Front 284

What are s/s of asthma?

Back 284

Expirational wheezing, shortness of breath, tightness in chest and coughing.

Front 285

What is Bronchiectasis?

Back 285

abnormal and irreversible dilatation of the bronchi and bronchioles proximal to the terminal brochioles w/ degeneration of elastic and muscular tissue d/t inflam. and accumulation of leukocytes.

Front 286

What are clinical factors of bronchiectasis?

Back 286

chronic cough; foul-smelling, large volume of sputum; fever

Front 287

What is cystic fibrosis?

Back 287

A hereditary disorder, abnormal viscous secretion of all the exocrine glands in the body.

Front 288

What glands are affected in cystic fibrosis and what does this lead to?

Back 288

Lung - lower respiratory infections Pancreas - steatorrhea (fatty stools)

Front 289

What are clinical factors of cystic fibrosis?

Back 289

increased thick mucus; decreased mucociliary clearance; increased bacterial infections

Front 290

What is chronic restrictive lung disease (CRPD)?

Back 290

Non-infectious disorder caused by dust characterized by diffuse fibrosis involving lung parenchyma.

Front 291

What is pneumoconiosis?

Back 291

An occupational dust Dz characterized by inhalation of organic dust, fumes, etc. a latent period b/w exposure and onset of clinical Dz

Front 292

What are the 4 classifications of pneumoconiosis?

Back 292

1. Anthracosis 2. Silicosis 3. Asbestosis 4. Berylliosis

Front 293

What is anthracosis?

Back 293

MC pneumoconiosis; coal worker's pneumoconiosis, exposure to carbon dust.

Front 294

What is Silicosis?

Back 294

Industrial worker's pneumoconiosis, exposure to grinding of stone, glass, sand, etc.

Front 295

What is Asbestosis?

Back 295

Most important pneumoconiosis; in brake linings, insulation, shipyard workers; increased risk of malignant mesothelioma and bronchogenic carcinoma.

Front 296

What is Beryllosis?

Back 296

A pneumoconiosis that is common in workers of the aerospace industry.

Front 297

What is sarcoidosis?

Back 297

A systemic disorder of idiopathic origin; commonly manifests in the lungs and lymph nodes and is associated w/ abnormalities of the immune system

Front 298

What are characteristics of sarcoidosis?

Back 298

non-casesating granulomas in lung and when they heal by organization lead to pulmonary fibrosis.

Front 299

What are clinical factors of sarcoidosis?

Back 299

Gradual onset of increasing dyspnea w/ hilar lymph node involvements.

Front 300

What 4 conditions have pulmonary fibrosis?

Back 300

1. TB 2. Pneumoconiosis 3. Goodpasture syndrome 4. Sarcoidosis

Front 301

What is Goodpasture syndrome?

Back 301

An interstitial lung and kidney disorder.

Front 302

What is goodpasture syndrome characterized by?

Back 302

hemoptysis, hematuria, anemia, pulmonary fibrosis, presence of circulating anti-glomerular basement membrane antibodies.

Front 303

What are risk factors for carcinoma of the lung?

Back 303

Cigarette smoking, beryllium, asbestose, radiation and a variety of genetic alterations.

Front 304

What are the well differentiated types of lung carcinoma?

Back 304

Squamous cell carcinoma and Adenocarcinoma

Front 305

Describe squamous cell carcinoma of the lung.

Back 305

MC type; near center of the lung; associated w/ smoking; silent until causes narrowing of bronchi; Arises from PSCC

Front 306

Describe Adenocarcinoma of the lung.

Back 306

Arises from pneumocytes; chest x-ray shows peripheral coin lesions (alveolar cancer)

Front 307

What are the undifferentiated types of lung carcinoma?

Back 307

Small cell carcinoma and Large cell carcinoma

Front 308

Describe small (oat) cell carcinoma.

Back 308

Arises from the neuroendocrine cells - highly malignant, fast growing, strongly associated w/ smoking; secretes ectopic hormones like ADH and ACTH (paraneoplastic syndrome)

Front 309

What are the pulmonary effects of undifferentiated types of lung carcinoma?

Back 309

cough, dyspnea, hemoptysis, chest pain, obstructive pneumonia, pleural effusion.

Front 310

What is pancoast syndrome?

Back 310

Involvement of lung apex by tumor may involve C8, T1, T2 nerves and can lead to Horner's syndrome where cervical sympathetic ganglions are affected.

Front 311

What is pneumothorax?

Back 311

Air in the pleural cavity.

Front 312

What are the clinical features of pneumothorax?

Back 312

Sudden pain or feeling of tightness on the affected side; affected by deep inspiration, sudden onset of severe dyspnea. Lead to severe respiratory distress.

Front 313

What is spontaneous pneumothorax?

Back 313

Air in the pleural cavity following the rupture of alveolus (inside - out)

Front 314

What is traumatic pneumothorax?

Back 314

Air in the pleural cavity following penetrating injuries to the chest (i.e. rib Fx)

Front 315

What is pleural effusion?

Back 315

collection of excess fluid in the pleural cavity d/t benign or malignant causes.

Front 316

What are the different types of pleural effusions and their causes? (5)

Back 316

1. Hydrothroax (heart failure patients) 2. Pyothorax (pus) and empyema (both complicated pneumonia) 3. Hemothorax (malignancy or trauma) 4. Chylothorax (lymphatic obstruction)

Front 317

What is malignant mesothelioma?

Back 317

Cancer of the pleura, d/t asbestos exposure. 15-20 years may elapse b/w exposure and dev. of tumor

Front 318

What are the predominant symptoms of malignant mesothelioma?

Back 318

Progressive chest pain and dyspnea; history of work

Front 319

3 METABOLIC diseases of heart

Back 319

HYPERthyroid (tachycardia, inc. workload, High output failure)

HYPOthyroid (bradycardia, slow output, myxedma, flabby, dilated, down cardiac output)

COBALAMIN DEFICIENCY (WET BERIBERI) = ALCOHOL consumption due to down vit B12)

Front 320

describe WET BERI BERI

Back 320

ALCOHOLISM
low B12 affects heart (cobalamin)

Front 321

EXAMPLE of ECCENTRIC DILATION

Back 321

IDOPATHIC DILATED CARDIOMYOPATHY

one right sided feature: BILATERAL PITTING PERIPHERAL EDEMA
one left sided feature: DYPSNEA

Front 322

RIGHT SIDED HEART FAILURE
MOST COMMON SYMPTOM

pg 7 for RVF features

Back 322

PERIPHERAL PITTING EDEMA

Front 323

LEFT SIDED HEART FAILURE
MOST COMMON SYMPTOM

pg. 5 for LVF features

Back 323

DYPSNEA

Front 324

Patient presents with bilateral pitting edema and dyspnea

Back 324

bilateral ventricular dilation and symmetrical hypertrophy

perhaps due to IDIOPATHIC DILATED CARDIOMYOPATHY or
MITRAL VALVE STENOSIS

Front 325

difference b/w
MITRAL VALVE STENOSIS
&
IDIOPATHIC DILATED CARDIOMYOPATHY

Back 325

MITRAL VALVE STENOSIS = RHEUMATIC FEVER history
vs
IDIOPATHIC DILATED CARDIOMYOPATHY = ALCOHOL history

both have bilateral ventricular dilation and symmetrical hypertrophy so have same presentation of bilateral peripheral pitting edema (RSHF) and dyspnea (LSHF)

Front 326

CARDIOMYOPATHY is due to

Back 326

ALCOHOL

Front 327

IDIOPATHIC HYPERTROPHIC SUBAROTIC STENOSIS
- IHSS

etiology

Back 327

AUTOSOMAL DOMINANT = no etiology. No dilation, only HYPERtrophy.

INTERVENTRICULAR SEPTUM ONLY hypertrophies

LEFT VENTRICLE mostly

YOUNG ADULT MALE

ANGINA, ATRIAL FIBRILLATION

SUDDEN DEATH

Front 328

what is hypertrophied in IHSS?

Back 328

INTERVENTRICULAR SEPTUM only

Front 329

HEMOCHROMATOSIS
AMYLOIDOSIS
SARCOIDOSIS

Back 329

RESTRICTED (NOT ABLE TO CONTRACT) cardiomyopathy - heart still able to contract but slow DIASTOLE/filling

due to iron or accumulation of protein

Front 330

Dressler's syndrome

Back 330

side effect of a myocardial infarct

Front 331

Most common cardiac tumor

Back 331

RHABDOMYOMA
(children)

Front 332

If a person has phaygitis, chorea (brain), skin rash, fever...Jone's criteria =

Back 332

Rheumatic fever

*can cause pericarditis (chest pain relieved by leaning forward)

Front 333

What causes a friction rub around the heart?

Back 333

PERICARDITIS

scratching sound is the cardinal sign of Rheumatic fever + fever

Front 334

bread and butter appearance

Back 334

pericarditis

Front 335

3 cardinal signs of pericarditis

Back 335

~fever

~chest pain (relieved leaning forward, agg. by laying down)

~ascultation (friction rub)

Front 336

accumulation of excess of fluid in pericardial cavity

Back 336

PERICARDIAL EFFUSION

can be exudate or transudate
N = 50ml, excess 350- 2L

Front 337

serous (failure)
chylous (lymph)
serosanguinous
hemo

Back 337

types of pericardium revealed by testing pericardial effusion/fluid

Front 338

difference b/w effusion and tamponade?

Back 338

effusion = slowly

tamponade = rapid

Front 339

water bottle appearance of heart on x-ray due to

Back 339

cardiac tamponade (rapid filling)

Front 340

BECK'S triad

Back 340

cardiac tamponade:

1. HYPOtension (no blood, no pressure)
2. increased VENOUS JUGULAR pressure (blood stays in vena cavas)
3. MUFFLED heart sounds (fluid b/w 2 layers of pericardium)

Front 341

CHRONIC FIBROSING disease from tuberculosis or radiation therapy to mediastinum

Back 341

CHRONIC CONSTRICTIVE PERICARDITIS

Front 342

TB = fibrous tissue = compression of heart =

Back 342

CONSTRICTIVE PERICARDITIS

Front 343

When do you use bio-prosthesis vs. mechanical?

Back 343

young female REPRODUCTIVE age

Front 344

When do you use a mechanical valve?

Back 344

older men and postmenopausal women

Front 345

Congenital disorders of respiratory tract: no symptoms, occasionally get infected.

Back 345

benign pulmonary CYST -

balloon like structure

Front 346

congenital disorder of respiratory tract: a portion of the lower lobe of lung separated from rest of lung but stays attached to AORTA

Back 346

pulmonary SEQUESTRATION

**board question

Front 347

congenital disorder of respiratory tract:
a communication between part of esophagus and trachea

Back 347

tracheo-esophageal FISTULA

causes ASPIRATION PNEUMONIA in infant

Front 348

congenital disorder of respiratory tract:
results in emphysema

Back 348

ALFA 1 ANTITRYSIN deficiency

Front 349

type 1 hypersensitivity reaction

Back 349

allergic rhinitis
dermatitis (poison ivy)
food poisoning

Front 350

why do we silmutaneously have ear itching, palate, nasal, sinus itching, watery eyes are all due to irritation of the

Back 350

TRIGEMINAL NERVE

type 1 hypersensitivity reaction

Front 351

frequent nasal discharge
cobblestone pharynx appearance
sensation of drainage
frequent clearing of throat

Back 351

POSTNASAL DRIP syndrome

Front 352

causes of laryngeal obstruction

Back 352

allergic edema
inhaled foreign body
inhaled vomitus
tumors of the larynx

Front 353

asphyxia

Back 353

swelling of larynx due to allergy

Front 354

Pulmonary hypertension
most common vascular problem:

Back 354

VSD ventral septal defect

also ASD

Front 355

Pulmonary hypertension type of stenosis:

Back 355

MITRAL VALVE stenosis

Front 356

Pulmonary obstructive disease:

Back 356

COPD

pulmonary artery enlarges, lungs enlarge, LUNG FAIL

Front 357

Dr. Jack Kevorkian died 6/4/11 of a

Back 357

pulmonary embolism

a broken free thrombus that either went to one lung or blocked both (his case = both)

Front 358

Most common blockage after surgery due to recumbancy

Back 358

pulmonary embolism

*that's why they make you walk immediately after fracture repair orthopedic surgery of a long bone

Front 359

Pulmonary embolism victims (4)

Back 359

1. orthopedic surgery
2. young reproductive age female taking birth control (d/t platelet aggregation)
3. fracture of a long bone
4. estrogen treatment in men for prostate cancer

Front 360

DVT sign

Back 360

Homan's sign for DVT

dorsiflexion of foot and causes pain in leg

(claudication is lying down)

Front 361

Describe path of pulmonary embolus:

Back 361

in leg
thrombus
embolus
to inferior vena cava
to right ventricle
to pulmonary artery
causes some blockage or all

Front 362

d/dx for MYOCARDIAL INFARCTION
VS.
PULMONARY EMBOLISM>

Back 362

no heart enzymes present in pulmonary embolism

Front 363

ARDS

Back 363

Acute Respiratory Distress Syndrome

sudden life threatening lung failure due to inflamed alveoli that ultimately collapse = no oxygen exchange

Front 364

Causes of ARDS

Back 364

sepsis
severe lung infection (viral or bacterial)
smoke or toxic fume inhalation
near drowning

Front 365

Lobar vs. broncho pneumonia

Back 365

Lobar = one side, one patch

Broncho = all over, diffuse

Front 366

Test for ARDS

Back 366

abnormal arterial blood gas content

Front 367

NRDS

Back 367

Neonatal Respiratory Distress Syndrome

*Hyaline Membrane Disease

Front 368

Describe NRDS

Back 368

PREmature infants (before 34 weeks gestation)
Hyaline membrane disease
TYpe II PNEUMOCYTES are immature so NOT ENOUGH SURFACTANT
tested via amniocentesis

Front 369

IN simple English, what is an abscess?

Back 369

boil

a cyst with a wall with something inside like pus, etc

Front 370

4 stages of pneumonia

Back 370

look them up

Front 371

consolidation of the lung

Back 371

solidification area in lung

sounds louder

Front 372

High fever symptoms

Back 372

shivering
rigor
chills

Front 373

Whenever there is an abcess in the body anywhere, there is a

Back 373

HIGH FEVER
shivering
rigor
chills

Front 374

Lung abcess due to BACTERIAL pneumonia goes to _________

Back 374

brain

Front 375

who has lung abscess

Back 375

young people drinking alcohol

Front 376

why foul smelling sputum?

Back 376

lung abcess

*duh, not brain!

Front 377

Describe lung ABCESS

Back 377

localized accumulation of pus

aspiration (choking on vomit) is common cause d/t ALCOHOL

cough, high fever, FOUL-SMELLING sputum belies lung abcess

Front 378

PRIMARY TB

Back 378

direct inhalation of M. tuberculosis

GHON'S FOCUS (peripheral parenchymal granuloma upper lobes)

GOHN'S COMPLEX focus and lymph node involvement

Heals by FIBROSIS or CALCIFICATION

5% becomes 2nd TB

Front 379

SECONDARY TB

Back 379

REACTIVIATION of primary TB

multiple granuloses

extensive necrosis

heals, calcifies, or erodes bronchus

TB cavity w/ CASEOUS NECROSIS

complications: MILIARY ( TB, HEMOPTYSIS

Front 380

may result in MILIARY TB

Back 380

Secondary TB

Front 381

why called tuberculosis?

why miliary tuberculosis?

Back 381

tubercles on surface

"seeds" on kidney, etc. tubercles everywhere on an organ

Front 382

COPD? CRPD?

Back 382

one is obstructive
one is restrictive

Front 383

includes chronic bronchitis, emphysema and asthma where there is DECREASED forced expiratory volume

Back 383

COPD

Front 384

difference in COPD & CRPD

Back 384

COPD - obstruction

CRPD - problem with interalveolar septum as restricting alveoli expansion

Front 385

If it's a DRY cough, it is not --------- bronchitis.

Back 385

chronic


*chronic has a productive cough
increase in sputum production
smoking

Front 386

Describe CHRONIC BRONCHITIS

Back 386

wet cough (steady increase in sputum and cough)
smoking
wheeze, dyspnea tightness esp. in morning

EXERTIONAL DYPSNEA, CYANOSIS OR COR PULMONALE

Front 387

derivatives of COPD

Back 387

Chronic bronchitis
Emphysema
(and asthma, accd to Boards)

Front 388

how to d/dx emphysema vs. chronic bronchitis

Back 388

emphysema: alveoli are broken down, BECOME ONE

LOSE SURFACE AREA

Front 389

Primary cause of emphysema

Back 389

Alpha 1 anti-trypsin deficiency


(2nd is cigarettes)

Front 390

Describe alpha 1 anti-trypsin deficiency

Back 390

not enough A1anti-trypsin to control the TRYPSIN which kills bacterial in the lungs

MAIN CAUSE OF EMPHYSEMA

Front 391

d/DX between emphysema and chronic bronchitis

Back 391

non-productive cough = emphysema

Front 392

chronic inflammatory disorder of airways
recurrent episodes of wheezing, breathlessness, chest tightness and coughing, esp at night

Back 392

asthma

Front 393

Condition of asthma

Back 393

BRONCHIAL TUBES in lungs react to different stimuli by BECOMING INFLAMED

Front 394

Asthma is a TYPE ___ hypersensitivity reaction

Back 394

ONE

Front 395

severe continuing attack of asthma

Back 395

status asthmaticus (lethal)

respiratory failure and death - continuous asthma

Front 396

sputum of asthmatic

Back 396

CUSHMAN'S SPIRALS
and CRYSTALS

Front 397

Bronchiectasis means:

Back 397

dilation of bronchi

irreversible
abnormal
chronic cough, foul smelling sputum w/ large volume, fever

Front 398

PROXIMAL problem before terminal bronchiole

Back 398

BRONCHIECTASIS

Front 399

DISTAL problem after terminal bronchiole

Back 399

EMPHYSEMA

Front 400

Inherited disorder that causes abnormal VISCUS SECRETION of all the EXOCRINE glands of body

Back 400

CYSTIS FIBROSIS

Front 401

point of mucus in respiratory and cillia?

Back 401

mucocilliary clearance

Front 402

Cystic fibrosis is when the _________ elevator crashes.

Back 402

mucocilliary elevator crash so increased bacterial infection

lung removal

Front 403

In case of male, cystic fibrosis causes ____________

Back 403

infertility

*sperm less

Front 404

CRPD

Back 404

chronic respiratory pulmonary disease
(same as CRLD)

Front 405

most important difference in COPD vs. CRPD

****test

Back 405

FEV1/VC is decreased in COPD but normal or increased in CRPD

Front 406

non-infectious disorder caused by dust characterized by diffuse fibrosis involving lung parenchym

Back 406

chronic RESTRICTIVE lung disease
CRLD

Front 407

CRPD is caused by

Back 407

DUST! caught in interalveolar septum that doesn't allow alveoli to expand

Front 408

types of chronic restrictive pulmonary disease

Back 408

pneumoconiosis
sarcoidosis
goodpasture's syndrome
carcinoma of lung

Front 409

occupational dust disease name and 4 types but just know definition

Back 409

PNEUMOCONIOSIS

anthracosis (anthrax)
silicosis (silicone)
asbestosis (asbestos)
beryliosis (berylium - aerospace)

Front 410

SARCOIDOSIS is lung and lymph nodes

Back 410

idiopathic

NON-CASEATING (tb is caseating) GRANULOMAS heal, fibrose and cause fibrosis

Increased dyspnea with hilar lymph node involvement

Front 411

SARCOIDOSIS is

**test

Back 411

Lung & lymph node


**TEST

Front 412

GOODPASTURE'S

Back 412

antibody against BASEMENT MEMBRANE OF:

KIDNEY & LUNG = fibrous tissue formation

Front 413

conditions to identify GOODPASTURES

**test

Back 413

hemoptysis (lung blood)
hematuria (kidney blood)

Front 414

Carcinoma of lung main cause

Back 414

cigarette smoking

1. squamous cell
2. adenocarinoma

Front 415

cancer from smoking starts in center of lung (hilus)

Back 415

SQUAMOUS CELL CARCINOMA

epithelial keratin PEARLS

Front 416

squamous cell carcinoma has

Back 416

epithelial keratin PEARLS

Front 417

Adenocarcinoma has

Back 417

peripheral COIN CELL lesions

from pneumocytes
non smokers

Front 418

Undifferentiated types of lung cancer:

Back 418

small / oat cell cancer
large cell cancer

Front 419

highly malignant cancer assoc. with smoking

Back 419

small/oat cell cancer

most patients die within a week to 6 weeks. Unstoppable.

Front 420

Clinical Features (CF) of cancers of lung:

Back 420

asymptomatic:
cough
dyspnea
hemoptysis
chest pain
obstructive pneumonia & pleural effusion

Front 421

Pancoast syndrome

Back 421

involve lung APEX
TUMOR may affect C8-T1 and 2 nerves

****ULNAR NERVE WEAKNESS****

Front 422

Horner's syndrome

Back 422

cervical sympathetic chain involvement:

miosis, ptosis, anhydrosis, enophthalmos

Front 423

SVC syndrome

Back 423

obstructs superior vena cava

Front 424

Metastasis

Back 424

regional nodes, brain, bone

Front 425

Paraneoplastic syndrome

Back 425

secrete ACTH and ADH -effects