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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
Q

R sided failure mnfts

A
  • abdominal organ distension
  • peripheral edema
  • fluid then moves into abdominal cavity which leads to ascites when there is a lack of interstitial space remaining
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26
Q

patho of L sided congestive heart failure

A

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

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27
Q

R sided heart failure
what is it
what results

A

failure to pump into pulmonary circuit leads to pooling in systemic circuit

mnft: peripheral edema and abdominal organ distension

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28
Q

L sided heart failure is

mnfts

A

failure to pump into systemic circuit leads to pooling in pulmonary circuit

mnft: pulmonary congestion and pulmonary edema

frothy sputum
activity intolerance
orthopnea

29
Q

how does compensated heart failure present

A

asymptomatically initially but eventualyt he compensation will lead to decompensation and then to failure

30
Q

Mechanisms of heart failure compensation

A
  1. ventricle dilation (Frank Starling Law)
  2. SNS
  3. Renin-Angiotensin
  4. ANP and BNP
  5. endothelins
  6. cardiac hypertrophy and remodelling
31
Q

what is the Frank Starling Law

A

inc EDV-> muscle stretch-> inc preload->inc CO

32
Q

how wil compesnation for heart failure using the fransk starling law negatively affect health

A

it can overstretch the heart

it inc the 02 requirements of the heart

33
Q

how does the SNS support a failing heart

A

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
Q

How does RAA compensate for heart failure

A

dec co ->dec renal perfusion-> RAAS triggered-> angiotensin II->aldosterone->hypervolemia->inc preload

35
Q

how does ANP and BNP affect heart failure

A

they are potent diuretics an natriuretics
they will affect vascular and smooth muscle

they act agains the others

36
Q

endothelins are made by

what do they cause

A

they are vasoconstrictors made by the endothelium (maybe lookup)
they cause smooth muscle proliferation and hypertrophy

37
Q

cardiac hypertrophy and remodelling

A

inc workload->hypertrophy
-eventually dec contractility
require more 02-> myocardial dyxfx

38
Q

can compensation for heart failure continue indefinitely

A

no.

39
Q

mnfts of HF

A

various
-effects of impaired pumping
initially it is asymptomatic until compensation fails

40
Q

dx of heart failure

A

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
Q

tx of heart failure
acute
chroic

if the defect is repairable

A

acute: stabilize & correct cause (see MI)

Chronic: symptomatic mgmt, dec risks and inc fx

sx for repairable defect

42
Q

if ejection fraction is > or equal to 40% what do in heart failure pt

A

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
Q

how to Tx pt w heart failure if they have symptoms at rest

A

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
Q

if ejection fraction is

A

if have systolic heart function with an ejection fraction of

45
Q

what is pericarditis

A

pericardial inflm d/t infection, injury

46
Q

patho of pericarditis

A

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
Q

when might cnstrictive pericarditis occur

A

fibrinous scar tissue

48
Q

mnfts of pericarditis

whats special abt this

A
  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
Q

tx of pericarditis

A

based on cause
anti inflm drugs
may use antibiotics if bacterial

50
Q

cardiac tamponade

A

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
Q

what type of shock can cardiac tamponade cause

A

obstructive shock (obstruction to filling

52
Q

mnft of cardac tamponade

A

dec co
dec arterial pressure
temporary tachycardia

any compensatory responses will change to decompensatory responses if it isnt working

53
Q

tx of cardiac tamponade

A

stat pericardiocentesis

aspirate the fluid in the pericardial space. if it is clotted then you cant use this method

54
Q

where do all blood cells originate from

A

pluripotent stem cells

55
Q

after the pluripotent stem cell how do the blood cells differentiate or divide

A

into lymphoid stem cells and myeloid stem cells

56
Q

after the myeloid and lymphoid stem cells how are the next cells different

A

the lymphoid stem cell turns into the NK, T, B cell progenitors whereas the myeloid are called coony forming units eg megakaryocyte CFU

57
Q

trace origin of basophil from pluripotent stem cell

A

p.s.c->myeloid stem cll->granulocyte CFU->basophil

58
Q

leukemia

A

proliferation of malignant leukoctes present in circulation

-that may infiltrate the tissue

59
Q

who does leukemia affect

A

most common CA in kids and young adults

but it is diagnosed 10x more freuently in adults than kids

60
Q

how is leukemis classified

A

as acute and chronic lyphocytic (lymphocytic) or myelogenous (onocytes, granulocytes) leukemia

61
Q

which form of leukemia has mature cells

A

the chronic, less aggressive form

62
Q

acute leukemia

A

has aggressive, immature blast cells

63
Q

etiology of leukemia

A

idiopathic (unsure of what alters the genes)

64
Q

risks for leukemia

A

genetic predisposition
lots of radiation
immunodeficiency
tcell leukemia virus

65
Q

how is the rest of the blood affected by leukemia

what does this result in?

A

the non-malignant blood cell production is also affected which leads to an impaired immune response and a dec 02 supply

66
Q

mnfts of leukemia

A

anemia, thrombocytopenia, leukopenia

  • bleeding gums
  • fever
  • generalized pain
  • fatigue
  • weakness, bruising
  • recurrent infection
67
Q

tx of leukemia

A

MCTACR
-radiation, chemo (often in combo)
-transfusions
-antimicrobials (viral, fungal bacterial maybe prophylactically)
colony stimulating factors (take growth factors)
-marrow transplant???

68
Q

what are the 3 phases of Tx of leukemia

A
  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
Q

how long might leukemia Tx have to continue

A

2 years

old patho 154 (18 decks)

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