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Patho > Cardiac > Flashcards

Cardiac Flashcards

1
Q

Causes of myocardial ischemia

A

Most common: atherosclerosis of coronary arteries. Also: severe htn or hypotension, tachycardia, hypoxia, anemia, severe AI/AS

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2
Q

RF mi

7

A 
Increasing age*
Males*
Increased LDL 
DM 
HTN
Smoking
Genetics
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3
Q

Other RF MI

A

Obesity, cerebrovascular disease, PVD, menopause, estrogen contraceptives, sedentary, nervous personality

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4
Q

Stable angina

A

No change in precipitating factors for at least 60 days. (Frequency/duration of pain)

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5
Q

Unstable angina

A

Caused by less than normal activity, lasts for prolonged period, occurs frequently, signals impending MI

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6
Q

Stable angina
Assoc w
02 demand
Relieved by

A

Fixed narrowing, 75% or more
Normal under basal conditions
Rest, reduce demand, vasodilator

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7
Q

Unstable angina

Characteristics
Can cause what

A

Crescendo, inc freq and duration
Can cause irreversible infarction
Acute plaque changes
Usually partial thrombosis

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8
Q

Prinzmetal angina

When occurs
What it is

A

At rest
Coronary spasm in a plaque area or normal vessel
Normally assoc w other vasospastic diseases like raynauds

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9
Q

Infarction

When it occurs
Begins where typically
Full size when
Size depends on

A

20-30 min of ischemia
Subendocardial areas
3-6h
Proximity of lesion and collateral circulation

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10
Q

Complications of MI

A

Papillary muscle dysfunc (valvular disease)
External rupture of infarct- day 4-7, tamponade/death
Mural thrombi- stroke
Acute pericarditis day 2-4
Ventricular aneurysm- most common in anteroapical region

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11
Q

Other complic MI

A 
Arrhythmia s 
LVF +/- pulmonary edema
Cardio genie shock (10%)
Rupture of wall, septum, or papillary muscle 
Thromboembolism
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12
Q

Cardiac microinfarctions do what

A

Raise troponin but not Ck mb

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13
Q

RCA occlusion affects what

A

Posterior/inferior LV

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14
Q

LCA occlusion affects what

A

Anterolateral, LV

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15
Q

LAD occlusion affects what

A

Anteroseptal, in between ventricles

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16
Q

LCX occlusion affects what

A

Lateral LV

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17
Q

What is vascular hypertension

A

Sustained 140/90

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18
Q

Normal bp
Prehypertension
Stage 1
Stage 2

A

<120/80
120-139 / 80-89
140-159 / 90-99
>160/>100

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19
Q

HTN most important RF for what

A 
CAD 
CVA
Cardiac hypertrophy 
Renal failure 
Aortic dissection
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20
Q

Types of hypertension

A

Essential- 95%

Secondary 5% due to:renal, endocrine, CV, neuro

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21
Q

BP = what components

A

CO (volume and cardiac factors)
X
Peripheral resistance (humoral- constrictors/dilatory, and neural factors)

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22
Q

RF essential htn

A

Genetic: polygenic, heterogenous, polymorphism in gene loci

Enviro: stress, obesity, smoking, salt, sedentary

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23
Q

Patho of htn

A

Inc SNS to stress
Over produc: vasoconstrictors, Na retaining hormones
Under produc: vasodilator, prostaglandins
Inc Na intake
Not enough Ca or K
DM, obesity

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24
Q

Pathogenesis of secondary htn

A 
Oral BC 
Renal parenchymal disease 
Renin secreting tumors 
Primary aldosteronism 
Cushing's 
Pheochromocytoma
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25
Q

Renovascular disease
Clinical findings
Labs

A

Epigastric or abd bruit
Severe htn in young pt

MRA
Aortography
Duplex ultrasonography
CT angio

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26
Q

Hyperaldosteronism

Clinical findings
Labs

A

Fatigue, weak, HA, parenthesis, nocturnal polyuria/dypsia

Urinary K, serum K, plasma renin and aldosterone

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27
Q

Aortic coarctation

Clinical findings
Labs

A

Elevated bp in upper limbs
Weak fem pulses
Systolic bruit

Aortography, echo, MRI, ct

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28
Q

Pheochromocytoma

Clinical findings
Labs

A

HA, palpitations, sweating, paroxysmal htn

Plasma metanephrines, urinary catecholamines, spot urine metanephrines, adrenal CT/MRI

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29
Q

Cushings

Clinical findings
Labs

A

Truncal obesity, proximal muscle weakness, purple striae, moon facies, hirsuitism

Dexamethasone suppression test
Urinary cortisol
Adrenal ct scan
Glucose tolerance test

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30
Q

Renal parenchymal disease

Clinical findings
Labs

A

Nocturia, edema

Urinary glucose/proteins/casts
Serum creatinine
Renal ultrasound
Renal biopsy

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31
Q

Pregnancy induced htn

Clinical findings
Labs

A

Peripheral/pulm edema
HA
Seizures
RUQ pain

Urinary protein, uric acid, CO, plt count

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32
Q

Htn tx

Drugs v non drugs

A

Diuretics first line

Reduce wt, stop smoking, activity, na, diets, no etoh, relax

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33
Q

Stage 1 htn drugs

A

Thiazides diuretics

Acei, arb, bb, Ccb, or combo

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34
Q

Stage 2 htn tx

A

Two drug combo usually thiazide diuretic and acei/bb/or Ccb

35
Q

Drugs for: prev mi

A

Ace inhib
Aldosterone antagonist
Bb

36
Q

HF drugs

A 
Ace i 
Aldosterone antagonist 
Arb
Bb
Diuretic
37
Q

Meds for high risk of CAD

A

Ace i
Bb
Ccb
Diuretic

38
Q

Meds for DM

A 
Ace i 
Arb 
Bb 
Ccb 
Diuretic
39
Q

Meds for ckd

A

Ace inhib

Arb

40
Q

Meds for recurrent stroke prevention

A

Ace inhib

Diuretic

41
Q

What is htn crisis

A

Sudden increase DBP over 130

Due to activation of RAA

42
Q

Treatment of hypertensive crisis

A

Reduce bp w Ntp 0.5-10 mcg/kg/min
Monitor UOP and ABP
Decrease DBP to 110-100 over several mins-hrs

43
Q

Mitral stenosis

Cause

A

Fusion of mitral valve leaflets at commissaries during healing of acute rheumatic fever

44
Q

Mitral stenosis

What happens in progression/symptoms

A

LA enlargement predisposes to afib. Stasis of blood in LA predisposes to thrombi. Need anticoagulant therapy

DOE when CO increased. CHF if severe

45
Q

Aortic stenosis patho

A

Non rheumatic usually from calcification and stenosis of congenitally abn bicuspid valve

Rheumatic as well, can occur w MVS

46
Q

Symptoms assoc w AS

A

Angina pectoris in absence of ischemic disease
DOE
Syncope

47
Q

Mitral regurg patho

A

Rheumatic fever, almost always w mitral stenosis

48
Q

Mitral regurg what happens

A

LA volume overload by retrograde flow of a pt of LV SV into LA

49
Q

Mitral regurg

What it does to PAOP

Significance

A

Regurgitant flow causes v wave on recording

Size of v wave correlates w magnitude of regurgitant flow

50
Q

Aortic regurg patho

A

Acute (infective, endocarditis, trauma, dissection of thoracic aneurysm)

Chronic (rheum fever, systemic htn)

51
Q

Aortic regurg

Hemodynamics issue

A

Regurg of part of ejected SV from aorta back into LV. Decrease in forward LV SV

52
Q

Dilated cardiomyopathy

Forms

Symptoms

A

Inflammatory/non-inflammatory

Early inflam: fatigue, dyspnea, palpitations

53
Q

Dilated CM

Late symptoms

Tx

A

CHF, pulsus alternans, tachycardia, pulmonary edema

Antibiotics

54
Q

Non inflammatory cm

Manifests as

Causes

A

CHF

Toxicity (alc) 
Idiopathic 
Degenerative 
Infiltration 
Post MI
55
Q

Non inflammatory dilated CM charac by

A

Elevated filling p
Failure of contractile strength
Inverse relationship b/w arterial impedance and stroke volume

56
Q

Clinical pic of CHF assoc w dilated CM

A

Forward failure:
Fatigue
Hypotension
Oliguria

57
Q

CM and CHF

All caused by

What happens w kidneys

A

Decreased CO and organ perfusion

Renal perfusion reduced, RAA activated, increases blood volume through na and h20 retention

58
Q

CM and CHF

Backward failure traits

A

Elevated filling pressures req by failing heart

Secondary mitral regurg caused by ventricular dilation

59
Q

CM and CHF left sided failure traits

A

Orthopnea
Pulm edema
Paroxysmal nocturnal dyspnea

60
Q

CM and CHF

Rt side failure charac by

A

Hepatomegaly
JVD
Peripheral edema

61
Q

Hypertrophic cardiomyopathy

4 names for it

A
  • Idiopathic hypertrophic subaortic stenosis (IHSS)
  • Asymmetric septal hypertrophy
  • Hypertrophic obstructive cardiomyopathy
  • Muscular subaortic stenosis
62
Q

Clinical features of hypertrophic cardiomyopathies

  • how you get it
  • most pts what
  • symptoms
A

Autosomal dominant trait- contractile elements of heart defective and inc in ca channels. Most pts asymptomatic, 1/2 present w cv arrest and death. Dyspnea, angina, syncope

63
Q

Hypertrophic CM
Heart rhythms
When pts symptomatic

A

Vfib mostly, SVTs and afib

20-30s

64
Q

Patho of hypertrophic CM

A 
Asymmetric myocardial hypertrophy
Diastolic dysfunc 
Enlarge of top of interventricular septum below aortic valve
Rapid LV ejec
Sub aortic pressure gradient
65
Q

Patho hypertrophic CM

Dynamic obstruction worsened by what

All produce what

A

Decreased preload and afterload, increased contractility

Reduction in ventricular volume, increasing proximity of anterior MV leaflet to IVs

66
Q

Hypertrophic CM

Factors that help improve systolic function

A

Impairing contractility
Volume loading
Vasoconstriction
Myocardial depression

67
Q

Hypertrophic CM

Most pts have some degree of what.

What worsens it
Poor __ compliance

A

MR. vasodilator worsen it, vasoconstrictors attenuate obstruction and decrease MR

Diastolic

68
Q

Hypertrophic CM

Imbalance in what

Medical management

A

Myocardial 02 reqs

Beta blockers (blunts sns mediated increases in subaortic stenosis and dec tachyarrythmias)

Ca channel blockers improves diastolic relaxation

69
Q

Hypertrophic CM

Tx and echo findings

A

Myomectomy

Thickened IVS base to apex
Poor septal motion
Anterior displacement of mitral valve

70
Q

Left to right shunt

Which conditions

Leads to what

A

ASD, VSD, PDA

Sometimes tardive cyanosis (w age) but no cyanosis from outset)

71
Q

ASD
Most common what
When formed, due to what, what happens

A

Cardiac malformation dx in adulthood
4-6 weeks in embryo
Foramen ovale not closing properly. Blood flows L to R atrium

72
Q

ASD clinical features

A

Eventually leads to pulm htn
Can cause reversal of R to L shunt- cause cyanosis and CHF
Can be assoc w mitral insufficiency

73
Q

VSD
Most common what
When develops
Can cause what

A

Heart defect at birth
4-8 weeks in gestation
May close spontaneously. Can cause L to R shunt, pulm htn, CHF, and endocarditis.
Surgery indicated

74
Q

PDA
Where/what it is
What is causes

A

Channel b/w PA and aorta, bypass of unox blood.
L to R shunt.
Pulm htn, cyanosis, CHF w bigger lesions, infective endocarditis

75
Q

Right to left shunts

Presentation
Causes

A

Cyanosis at birth. Poorly 02 blood from right side of heart introduced directly into arterial circ via L heart
Tet of fallot and transposition of great vessels

76
Q

Tet of fallot
Most common what
Caused by what

A

Cause of cyanotic congenital heart disease

Abn division of truncus arteriosus into a pulm trunk and aortic root

77
Q

Components of tet of fallot

A

VSD
Dextraposed aortic root that overrides the VSD
RV outflow obstruction
RV hypertrophy

78
Q

TET

Clinical signs

A

R to L shunt
Dec flow to lungs, inc flow to aorta
Extent of shunting depends on degree of outflow obstruction

79
Q

TET
Tx

Manifestations/due to what

A

Surgical repairs
Chronic cyanosis
Erythrocytosis, inc blood viscosity, digital clubbing, infective endocarditis, systemic emboli, brain abscesses

80
Q

Transposition of great vessels
Anatomical variation
Features
Survival

A

Aorta rises from RV, PA from LV. Cyanosis.

Need ASD, VSD, PDA to survive at birth

81
Q

Coarctation of aorta

What happens.
More common in whom
Named due to
More common type

A

Abn aortic narrowing
Males
Pre or postductal, where in relation to ductus arteriosus
Post ductal

82
Q

Predictable COA

Presentation

A 
Infantile
Weak femoral pulses
Cyanosis in lower extremities 
CHF 
Need surgical correction to survive
83
Q

Postductal COA

Presentation

A

Older kids/young adults
Collaterals develop
Decreased perfusion to kidneys, RAS activated
Higher pressures upper extrem, lower in lower
Intermittent claudication may arise

Patho (11 decks)

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