Endocarditis-leukemia Flashcards
endocarditis is in most cases
a bacterial infection of endocardium and valves that leads to inflm
2 requirements to acquire endocarditis
- microbe must enter CVS and survie
2. adherence surface eg defective valves
where do the bacteria colonize in endocardities
amongs the platelets and fibrin
mnft of endocarditis
those of local and systemic infection impaired heart fx -L valvular dysfx distal embolization?? may not occur murmur
IH.LV.EM
infection.Heart fx, L Valve fx, Embolization. Murmur
how to diagnose edocarditis
culture and sensitivity of blood ad echocardiogram
Tx of endocarditis
eradicate the microbe with antibiotics
(address?) cardiac complications
when does rheumatic heart disease dev
during rheumatic fever
what is rheumatic fever
immune mediated inflm
acute, multi system
inflm of the valves, myocardium, pericardium
who does rheumatic fever target most
approx 3% of those age 5-15
what precedes rheumatic fever
a bacterial pharyngeal infection that lasts 1-4wks
how does rheumatic fever cause problems beyond inflm
acute multi system immune mediated inflammation
the body mounts an IR to deal w infxn and deals w the pathogen. The IR changes and begins to target self-ag
(his notes) target Ags in the heart, joints, CNS and inteument (molecular mimicry)
rheumatic heart disease leads to what
inflm of the valves, myocardium, pericardium
if chroni can lead to severe heart damage
how serious is rheumatic fever
most of the time the kid gets over it
the acute form is self limiting
Tx of rheumatic heart disease
- penicillin or erythromycin
- anti inflammatory drug
- dec cardiac work load by bed rest
- symptomatic mgmt
- complications
Congestive heart failure is
how long can pt survive w this
the endpoint of serious heart disease
-pt can survive w congestive heart failure for years
what does the congestive in CHF refer to
the congestion of blood within blood vessels. it is pooling and moving slowly
what are the three primary areas of congestion in CHF
- inside the heart (not coronary circuit)
- pulmonary circuit
- systemic circuit
Et LOOKUP RISK FACTORS PG 584. ARE THEY DIFF THAN ONES BEFORE OR COMMON
HTN DIABETES TYPE 2\ SMOKING OBESITY OLDER AGE SEX PHYSICAL INACTIVITY ischemic heart disease hyperlipidemia ethnicity heavy alcohol use excessive salt intake cardiotoxic agents FAMILY HISTORY/GENETIC MARKERS impired diastolic function L ventricular hypertrophy elevated neurohormonal biomarkers abnormal ECG microabluminouria elevated resting heart rate
caps are common but not sure abt inactivity
(some) Etiology of CHF
- MI
- cardiomyopathy (lookup which one
- highly in cardiac work load
- valvular disease
- hypervolemia eg Ivs
- uncontrolled HTN
- normal resting Co can inc 5 fold normally but in a weak heart theres limited response
The failure can begin on either side but we will assum L ventricle failure here.
what would happen if normal CO of 200 but now can only pump 125
theres 75ml residual volume in the ventricle. There will also be 75ml residual volume in atrium. They both must work hard and this leads to hypertrophy.
-the pulmonary return wont be complete as theres residual volue in hte right atrium which leads to congestion in the pulmonary veins
what will L sided failure cause to R side
R sided failure eventually
Lookup DOES R SIDED FAILURE LEAD TO L SIDED FAILURE
l elsewhere in my notes I said that it does
2 primary manifestions of L sided heart failure
- pulmonary congestion (always in the vessels)
- pulmonary edema
where is congestion in a circuit
in the place that youre receiving from
R sided failure mnfts
- abdominal organ distension
- peripheral edema
- fluid then moves into abdominal cavity which leads to ascites when there is a lack of interstitial space remaining
patho of L sided congestive heart failure
LV doesnt eject sufficient volume-> resiudal volume in lV-> left Atrium pumps harder to empty blood into LV->fails to empty fully-> LA unable to receive pulmonary return-> pulmonary congestion and pulmonary edema-> RV workload increases and->RV hypertrophy
RV failur usually follows LV failure
R sided heart failure
what is it
what results
failure to pump into pulmonary circuit leads to pooling in systemic circuit
mnft: peripheral edema and abdominal organ distension
L sided heart failure is
mnfts
failure to pump into systemic circuit leads to pooling in pulmonary circuit
mnft: pulmonary congestion and pulmonary edema
frothy sputum
activity intolerance
orthopnea
how does compensated heart failure present
asymptomatically initially but eventualyt he compensation will lead to decompensation and then to failure
Mechanisms of heart failure compensation
- ventricle dilation (Frank Starling Law)
- SNS
- Renin-Angiotensin
- ANP and BNP
- endothelins
- cardiac hypertrophy and remodelling
what is the Frank Starling Law
inc EDV-> muscle stretch-> inc preload->inc CO
how wil compesnation for heart failure using the fransk starling law negatively affect health
it can overstretch the heart
it inc the 02 requirements of the heart
how does the SNS support a failing heart
it aims to inc Co
- vasoconstriction=inc resistance in vessels->inc P-> inc preload->inc Co
- tachycardia-inc HR->CO
- inc contractility-> more volume
How does RAA compensate for heart failure
dec co ->dec renal perfusion-> RAAS triggered-> angiotensin II->aldosterone->hypervolemia->inc preload
how does ANP and BNP affect heart failure
they are potent diuretics an natriuretics
they will affect vascular and smooth muscle
they act agains the others
endothelins are made by
what do they cause
they are vasoconstrictors made by the endothelium (maybe lookup)
they cause smooth muscle proliferation and hypertrophy
cardiac hypertrophy and remodelling
inc workload->hypertrophy
-eventually dec contractility
require more 02-> myocardial dyxfx
can compensation for heart failure continue indefinitely
no.
mnfts of HF
various
-effects of impaired pumping
initially it is asymptomatic until compensation fails
dx of heart failure
history and physcial exam in which you take note of risk factors
labs eg CBC, electrolytes, liver fx (liver will be distended if HF)
ecg, echocardiogram
tx of heart failure
acute
chroic
if the defect is repairable
acute: stabilize & correct cause (see MI)
Chronic: symptomatic mgmt, dec risks and inc fx
sx for repairable defect
if ejection fraction is > or equal to 40% what do in heart failure pt
treat the cause eg HTN
use ACE I and may or may not need B blocker
if symptomatic w activity use angiotensin receptor blocker
how to Tx pt w heart failure if they have symptoms at rest
inc the dose of their ACE I, B blocker and Angiotensisn receptor blocker? or aybe just the angiotensisn receptor blocker
or may add diuretic
if ejection fraction is
if have systolic heart function with an ejection fraction of
what is pericarditis
pericardial inflm d/t infection, injury
patho of pericarditis
the inflm->inc cap permb->exudate in pericardial space
this exudate will travel to area of least resistance which is pericardial space.
fibrinous or fluid exudate that restricts cardiac fx by application of external P
the pericardial fluid may be displaced
when might cnstrictive pericarditis occur
fibrinous scar tissue
mnfts of pericarditis
whats special abt this
- chest pain (inc by respirations or movement) the l lung is adjacent to pericarium which is injured and causes pain. movement also causes rubbing agains the heart
- pericardial rub-hear a sound indicating friction
- ECG changes
tx of pericarditis
based on cause
anti inflm drugs
may use antibiotics if bacterial
cardiac tamponade
tamponade refers to external compression of heart d/t accumulation of fluid, pus, air in pericardial space
this restricts filling and emptying and is life threatening
what type of shock can cardiac tamponade cause
obstructive shock (obstruction to filling
mnft of cardac tamponade
dec co
dec arterial pressure
temporary tachycardia
any compensatory responses will change to decompensatory responses if it isnt working
tx of cardiac tamponade
stat pericardiocentesis
aspirate the fluid in the pericardial space. if it is clotted then you cant use this method
where do all blood cells originate from
pluripotent stem cells
after the pluripotent stem cell how do the blood cells differentiate or divide
into lymphoid stem cells and myeloid stem cells
after the myeloid and lymphoid stem cells how are the next cells different
the lymphoid stem cell turns into the NK, T, B cell progenitors whereas the myeloid are called coony forming units eg megakaryocyte CFU
trace origin of basophil from pluripotent stem cell
p.s.c->myeloid stem cll->granulocyte CFU->basophil
leukemia
proliferation of malignant leukoctes present in circulation
-that may infiltrate the tissue
who does leukemia affect
most common CA in kids and young adults
but it is diagnosed 10x more freuently in adults than kids
how is leukemis classified
as acute and chronic lyphocytic (lymphocytic) or myelogenous (onocytes, granulocytes) leukemia
which form of leukemia has mature cells
the chronic, less aggressive form
acute leukemia
has aggressive, immature blast cells
etiology of leukemia
idiopathic (unsure of what alters the genes)
risks for leukemia
genetic predisposition
lots of radiation
immunodeficiency
tcell leukemia virus
how is the rest of the blood affected by leukemia
what does this result in?
the non-malignant blood cell production is also affected which leads to an impaired immune response and a dec 02 supply
mnfts of leukemia
anemia, thrombocytopenia, leukopenia
- bleeding gums
- fever
- generalized pain
- fatigue
- weakness, bruising
- recurrent infection
tx of leukemia
MCTACR
-radiation, chemo (often in combo)
-transfusions
-antimicrobials (viral, fungal bacterial maybe prophylactically)
colony stimulating factors (take growth factors)
-marrow transplant???
what are the 3 phases of Tx of leukemia
- induction (trying to induce remmission
- intensification (intensifying the remission by inc the dose)
- maintenance (you maintain the remission by dec dose
how long might leukemia Tx have to continue
2 years
