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Flashcards in Endocarditis-leukemia Deck (69):
1

endocarditis is in most cases

a bacterial infection of endocardium and valves that leads to inflm

2

2 requirements to acquire endocarditis

1. microbe must enter CVS and survie
2. adherence surface eg defective valves

3

where do the bacteria colonize in endocardities

amongs the platelets and fibrin

4

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

5

how to diagnose edocarditis

culture and sensitivity of blood ad echocardiogram

6

Tx of endocarditis

eradicate the microbe with antibiotics
(address?) cardiac complications

7

when does rheumatic heart disease dev

during rheumatic fever

8

what is rheumatic fever

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

9

who does rheumatic fever target most

approx 3% of those age 5-15

10

what precedes rheumatic fever

a bacterial pharyngeal infection that lasts 1-4wks

11

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)

12

rheumatic heart disease leads to what

inflm of the valves, myocardium, pericardium
if chroni can lead to severe heart damage

13

how serious is rheumatic fever

most of the time the kid gets over it

the acute form is self limiting

14

Tx of rheumatic heart disease

-penicillin or erythromycin
-anti inflammatory drug
-dec cardiac work load by bed rest
-symptomatic mgmt
-complications

15

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

16

what does the congestive in CHF refer to

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

17

what are the three primary areas of congestion in CHF

-inside the heart (not coronary circuit)
-pulmonary circuit
-systemic circuit

18

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

19

(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

20

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

21

what will L sided failure cause to R side

R sided failure eventually

22

Lookup DOES R SIDED FAILURE LEAD TO L SIDED FAILURE

l elsewhere in my notes I said that it does

23

2 primary manifestions of L sided heart failure

-pulmonary congestion (always in the vessels)
-pulmonary edema

24

where is congestion in a circuit

in the place that youre receiving from

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