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old patho 154 > Endocarditis-leukemia > Flashcards

Endocarditis-leukemia Flashcards

1
Q

endocarditis is in most cases

A

a bacterial infection of endocardium and valves that leads to inflm

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2
Q

2 requirements to acquire endocarditis

A
  1. microbe must enter CVS and survie

2. adherence surface eg defective valves

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3
Q

where do the bacteria colonize in endocardities

A

amongs the platelets and fibrin

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4
Q

mnft of endocarditis

A 
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

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5
Q

how to diagnose edocarditis

A

culture and sensitivity of blood ad echocardiogram

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6
Q

Tx of endocarditis

A

eradicate the microbe with antibiotics

(address?) cardiac complications

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7
Q

when does rheumatic heart disease dev

A

during rheumatic fever

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8
Q

what is rheumatic fever

A

immune mediated inflm
acute, multi system
inflm of the valves, myocardium, pericardium

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9
Q

who does rheumatic fever target most

A

approx 3% of those age 5-15

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10
Q

what precedes rheumatic fever

A

a bacterial pharyngeal infection that lasts 1-4wks

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11
Q

how does rheumatic fever cause problems beyond inflm

A

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)

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12
Q

rheumatic heart disease leads to what

A

inflm of the valves, myocardium, pericardium

if chroni can lead to severe heart damage

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13
Q

how serious is rheumatic fever

A

most of the time the kid gets over it

the acute form is self limiting

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14
Q

Tx of rheumatic heart disease

A
  • penicillin or erythromycin
  • anti inflammatory drug
  • dec cardiac work load by bed rest
  • symptomatic mgmt
  • complications
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15
Q

Congestive heart failure is

how long can pt survive w this

A

the endpoint of serious heart disease

-pt can survive w congestive heart failure for years

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16
Q

what does the congestive in CHF refer to

A

the congestion of blood within blood vessels. it is pooling and moving slowly

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17
Q

what are the three primary areas of congestion in CHF

A
  • inside the heart (not coronary circuit)
  • pulmonary circuit
  • systemic circuit
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18
Q

Et LOOKUP RISK FACTORS PG 584. ARE THEY DIFF THAN ONES BEFORE OR COMMON

A 
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

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19
Q

(some) Etiology of CHF

A
  • 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
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20
Q

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

A

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

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21
Q

what will L sided failure cause to R side

A

R sided failure eventually

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22
Q

Lookup DOES R SIDED FAILURE LEAD TO L SIDED FAILURE

A

l elsewhere in my notes I said that it does

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23
Q

2 primary manifestions of L sided heart failure

A
  • pulmonary congestion (always in the vessels)

- pulmonary edema

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24
Q

where is congestion in a circuit

A

in the place that youre receiving from

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25
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
26
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
27
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
28
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
29
how does compensated heart failure present
asymptomatically initially but eventualyt he compensation will lead to decompensation and then to failure
30
Mechanisms of heart failure compensation
1. ventricle dilation (Frank Starling Law) 2. SNS 3. Renin-Angiotensin 4. ANP and BNP 5. endothelins 6. cardiac hypertrophy and remodelling
31
what is the Frank Starling Law
inc EDV-> muscle stretch-> inc preload->inc CO
32
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
33
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
34
How does RAA compensate for heart failure
dec co ->dec renal perfusion-> RAAS triggered-> angiotensin II->aldosterone->hypervolemia->inc preload
35
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
36
endothelins are made by | what do they cause
they are vasoconstrictors made by the endothelium (maybe lookup) they cause smooth muscle proliferation and hypertrophy
37
cardiac hypertrophy and remodelling
inc workload->hypertrophy -eventually dec contractility require more 02-> myocardial dyxfx
38
can compensation for heart failure continue indefinitely
no.
39
mnfts of HF
various -effects of impaired pumping initially it is asymptomatic until compensation fails
40
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
41
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
42
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
43
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
44
if ejection fraction is
if have systolic heart function with an ejection fraction of
45
what is pericarditis
pericardial inflm d/t infection, injury
46
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
47
when might cnstrictive pericarditis occur
fibrinous scar tissue
48
mnfts of pericarditis | whats special abt this
1. 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 2. pericardial rub-hear a sound indicating friction 3. ECG changes
49
tx of pericarditis
based on cause anti inflm drugs may use antibiotics if bacterial
50
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
51
what type of shock can cardiac tamponade cause
obstructive shock (obstruction to filling
52
mnft of cardac tamponade
dec co dec arterial pressure temporary tachycardia any compensatory responses will change to decompensatory responses if it isnt working
53
tx of cardiac tamponade
stat pericardiocentesis aspirate the fluid in the pericardial space. if it is clotted then you cant use this method
54
where do all blood cells originate from
pluripotent stem cells
55
after the pluripotent stem cell how do the blood cells differentiate or divide
into lymphoid stem cells and myeloid stem cells
56
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
57
trace origin of basophil from pluripotent stem cell
p.s.c->myeloid stem cll->granulocyte CFU->basophil
58
leukemia
proliferation of malignant leukoctes present in circulation | -that may infiltrate the tissue
59
who does leukemia affect
most common CA in kids and young adults but it is diagnosed 10x more freuently in adults than kids
60
how is leukemis classified
as acute and chronic lyphocytic (lymphocytic) or myelogenous (onocytes, granulocytes) leukemia
61
which form of leukemia has mature cells
the chronic, less aggressive form
62
acute leukemia
has aggressive, immature blast cells
63
etiology of leukemia
idiopathic (unsure of what alters the genes)
64
risks for leukemia
genetic predisposition lots of radiation immunodeficiency tcell leukemia virus
65
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
66
mnfts of leukemia
anemia, thrombocytopenia, leukopenia - bleeding gums - fever - generalized pain - fatigue - weakness, bruising - recurrent infection
67
tx of leukemia
MCTACR -radiation, chemo (often in combo) -transfusions -antimicrobials (viral, fungal bacterial maybe prophylactically) colony stimulating factors (take growth factors) -marrow transplant???
68
what are the 3 phases of Tx of leukemia
1. induction (trying to induce remmission 2. intensification (intensifying the remission by inc the dose) 3. maintenance (you maintain the remission by dec dose
69
how long might leukemia Tx have to continue
2 years

old patho 154 (18 decks)

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