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Advanced Pathophysiology > CVD & Obesity > Flashcards

CVD & Obesity Flashcards

Exam III

1
Q

BP equation

A

CO x PVR

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2
Q

CO equation

A

HR x SV

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3
Q

SV components

A

Preload
Contractility
Afterload (arterial vessel diameter)

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4
Q

PVR components

A

Blood viscosity
Afterload (arterial vessel diameter)

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5
Q

Preload components

A

Fluid volume
Venous vessel diameter

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6
Q

Humoral regulation

A

Vasodilators
BNP & ANP
NO
Prostacyclin
Endothelins

Vasoconstrictors
Epi & norepi
ADH
Angiotensin II

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7
Q

HTN

A

Persistent elevation in systolic OR diastolic blood pressure due to an increase in cardiac output, peripheral resistance, or both.

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8
Q

Hyaline Sclerosis

A

Hardening and stiffening of arterioles due to accumulation of hyaline (glass like) proteins

Hypertension of aging

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9
Q

Leading cause of death in the US

A

heart disease

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10
Q

Atherosclerosis

A

Hardening due to accumulation of plaque/lipids in the arteries

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11
Q

Primary HTN and the pressure-natriuresis curve

A

Shifts curve to the right

Meaning: a higher pressure is required to excrete salt compared to a person with normal blood pressure (they retain salt)

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12
Q

Contributors to HTN

A

Obesity;
SNS, RAAS, and natriuretic hormone dysfunction;
Inflammation

—>

Vasoconstriction and renal salt/fluid retention

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13
Q

Adipocytes characteristics and effects

A

Store triglycerides as one drop

Hyperplasia and hypertrophy in obesity

Increase angiotensinogen synthesis

Secrete leptin (with leptin resistance)

Inhibit adiponectin

Increase inflammatory mediators

Increase FFAs

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14
Q

Adipokines

A

Hormones produced by adipocytes

Autocrine, paracrine, and endocrine functions:

Control of food intake and energy expenditure

Lipid storage

Insulin sensitivity

Immune and inflammatory response

Coagulation, fibrinolysis, angiogene

Fertility vascular homeostasis

BP regulation

Bone metabolism

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15
Q

Adipokines increased in obesity

A

Angiotensinogen

Angiotensin type 1 and 2 receptors

Renin

ACE

Leptin

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16
Q

Adipokine decreased in obesity

A

Adiponectin

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17
Q

Leptin

A

Responsible for satiety
Stimulates energy expenditure
Upregulates the SNS in the brain (sympathoactivation)
Insulin sensitizer for skeletal muscle and liver
Plays a modulating role in reproduction, angiogenesis, immune response, BP control, and osteogenesis
Pro-inflammatory

Obesity associated w leptin resistance

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18
Q

Orexigenic neurons

A

Increase appetite
Decrease metabolism

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19
Q

Anorexigenic neurons

A

Suppress appetite
Increase metabolism

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20
Q

Adiponectin

A

Increases insulin sensitivity
Antiatherogenic
Anti-inflammatory
Increases NO release

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21
Q

HTN Dx

A

Based on averages of two blood pressures on two separate occasions

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22
Q

US vs European HTN tx

A

US/AHA:
>130/80 definition
ACE-I, CCB, and Diuretics are first line tx; BB are second line

Europe/ESH:
>140/90 definition
BB included as first-line therapy

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23
Q

Chronic HTN manifestations

A

Mostly asymptomatic until end organ damage has occurred to the arteries/arterioles of eyes, kidney, heart, & brain

Gradual loss of visual acuity
CKD
Cardiomyopathy, HF
Dementia

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24
Q

HTN crisis

A

Acute development of severe hypertension (>180 and/or >120) that causes acute end organ complications

Retinal hemorrhages (visualized by ophthalmoscopic exam), papilledema, blindness
AKI
ACS
CVA

Treat by gradual reduction in BP over 24-36 hours

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25
Q

Atherosclerosis definition

A

The hardening (sclerosis) of the arteries by atheromatous (low density lipoprotein = LDL) plaque

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26
Q

Atherosclerosis causes

A

Endothelial cell injury from
1. uncontrolled HTN
2. smoking
3. hyperlipidemia

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27
Q

Inflammatory response leading to atherosclerosis

A

Subendothelial accumulation of LDL cholesterol activates the inflammatory response

This oxidizes the LDL

The oxidized LDL activates adhesion molecules for monocytes (further increasing inflammation)

Monocyte differentiates into ingesting macrophage

The macrophage penetrates the endothelium, where it engulfs and oxidizes LDL cholesterol

Foam cells create a fatty streak

The fatty streak forms an atherosclerotic plaque

Smooth muscle covers the plaque

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28
Q

Stable atherosclerosis

A

Has a small lipid core and thick, calcified cap

Unlikely to rupture, but size will OCCLUDE the blood vessel

Typical cause of stable angina

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29
Q

Unstable atherosclerosis

A

Has a large lipid core and thin, friable cap

Ruptures easily, allowing contents to leak and cause a blood clotting response –> thrombus formation

Can cause acute arterial occlusion and acute coronary syndrome

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30
Q

Lipoprotein components

A

Triglycerides
Cholesterol
Phospholipids
Apolipoprotein

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31
Q

HDL

A

Good cholesterol
Anti-atherogenic

Desired level > 60

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32
Q

LDL and VLDL

A

Bad cholesterol
Pro-atherogenic

LDL desired level <100

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33
Q

LDL-lipoprotein A
Apolipoprotein

A

Very bad cholesterol
Proatherogenic, increases the adherence of LDL to vessel walls

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34
Q

Dyslipidemia

A

Hypercholesterolemia
General cholesterol levels do not address the relative risk for a patient developing atherosclerotic disease

35
Q

Triglyceride levels

A

Desired <150

*Fasting

36
Q

Total cholesterol level

A

Desired <200

37
Q

Atherosclerosis risk stratified cholesterol guidelines

A

More clinically relevant

Risks drive treatment with LDL targets

Risks: very high LDL, diabetes mellitus, and existing atherosclerotic disease

38
Q

Primary prevention of atherosclerotic cardiovascular disease (ASCVD)

A

No hx of MI or CVA

**Treat if:
LDL is very high
DM
10 year risk is >%75

39
Q

DM and atherosclerosis

A

An accelerator to atherosclerosis, regardless of cholesterol levels

40
Q

Secondary prevention of ASCVD

A

Clinical atherosclerotic disease

Goal: reduce cholesterol levels to LDL <70 or by 50%

41
Q

Atherosclerosis complications

A

Cerebrovascular disease
Peripheral arterial disease
Coronary artery disease

42
Q

L main carotid artery

A

Short and truncated

Divides almost immediately into the left circumflex and the left anterior descending coronary arteries

43
Q

RCA

A

Provides arterial blood to the RV and inferior heart

44
Q

White adipose tissue (WAT) characteristics

A

Visceral and subcutaneous

Physiologic functions:
Coagulation
Immunity
Appetite regulation
Glucose and lipid metabolism
Reproduction
Angiogenesis
Fibrinolysis
Body weight homeostasis
Vascular tone control

Visceral WAT normally hypertrophies, resulting in:
Insulin resistance (diabetes),
inflammation (DM, cancer, atherosclerosis),
Altered lipids (NAFLD/NASH, atherosclerosis),
Renin and angiotensin increase (HTN)

Subject to hormones (esp estrogen)

Metabolically active

45
Q

Lipotoxicity

A

Tissue exceeds supporting vascular supply, leading to cell necrosis and increased inflammation

46
Q

Beige adipose tissue (bAT)

A

“Brown in white”

Develops within WAT following:
Chronic exposure to cold (but reverts back to WAT with warm adaptation)
Exercise
Exposure to synthetic ligan of peroxisome proliferator-activated receptor-y (PPARy; “Pee-par-gamma”) or thiazolinediones (TZD)

Increased bAT is a promising target for obesity tx

47
Q

Bone marrow adipose tissue (MAT):

A

Found mostly in long bones

Metabolically active

Releases adipokines

Excess is associated with osteoporosis (takes up space of the bone)

Last fat to be used for energy (Starvation states; chronic negative energy balance)

48
Q

Obesogens

A

Chemicals in our environment that stimulate the development of fat/obesity

Epigenetic influences
Disrupt hormone signals
Cross the placenta and are in breastmilk
Passed down through generations

49
Q

Hypothalamus role in food intake

A

Regulates food intake and energy metabolism through orexigenic and anorexigenic neurons

Controls reward, pleasure, memory, and addictive behavior

50
Q

Medical conditions predisposing to obesity

A

Cushing syndrome
PCOS
GH deficiency
Hypothyroidism

51
Q

Anorexia of aging related factors

A

○ Reduced energy needs
○ Waning hunger
○ Diminished sense of taste and smell
○ Decreased production of saliva
○ Altered GI satiety mechanisms
○ Co-morbidities
○ Medications
○ Decreased orexigenic and increased anorexigenic signals
○ Delayed gastric emptying
○ Decreased small intestine motility
○ Sensory impairments
○ Medical/psychiatric disorders
○Social isolation, abuse, neglect

52
Q

Causes of cardiac ischemia (myocardial oxygen deficit)

A
  1. Increased demands
    □ Exercise
    □ Valvular disease (esp. aortic narrowing)
    ® Heart must generate higher pressure to move blood through stenotic valves
    □ Hemodynamic abnormalities
    ® Increased preload
    ® Increased PVR
  2. Insufficient supply
    □ Plaque or thrombus
    □ Anemia
    □ Hypoxemia
    □ Hypotension
53
Q

Stable angina

A

Stable atherosclerosis and cap

CP is predictable; induced by exercise and relieved by rest/nitrates
Demand ischemia

No necrosis
NOT an ACS
Negative troponin

54
Q

ECG changes with stable angina, unstable angina, and NSTEMI

A

transient ST segment depression and T wave inversion

55
Q

Acute coronary syndromes

A

Transient ischemia – Unstable angina
Sustained ischemia – MI (N-STEMI or STEMI)

Involve cardiac infarction (manifestation of tissue necrosis)
Almost always characterized by thrombus formation

56
Q

Ischemia cellular pathophysiology

A

Intracellular myocyte ion dysregulation:
□ Na­­+ and Ca++ accumulate inside the cell → myocyte swelling and cell wall damage
□ Dysregulated ions → electrophysiologic abnormalities (especially reentry circuits) → dysrhythmias (ventricular fibrillation)

Neurotransmitter and hormonal responses:
□ Catecholamines (norepinephrine and epinephrine) increase free fatty acids (FFA)
® FFA have detergent effect on myocyte membrane → cell wall damage (break down phospholipids)
□ Norepinephrine and angiotensin II → vasoconstriction → decreased coronary blood flow

57
Q

Unstable angina

A

Unpredictable CP occurring at rest and increasing in frequency (usually resolves, but can progress to NSTEMI)

Myocardial injury
+ HIGH SENSITIVITY troponin (HS3 cTnl)

58
Q

NSTEMI

A

MI and its associated acute CP

Subendocardial ischemia and necrosis

+ troponin

59
Q

MI chest pain

A

Unpredictable, sudden, severe, crushing

Radiates to jaw, neck, shoulder, L arm

Usually associated with anxiety, N/V, indigestion

may also have anginal equivalents

60
Q

STEMI ECG changes

A

ST segment elevation

Resolves in time and patient develops pathological Q wave

61
Q

STEMI

A

Transmural ischemia and necrosis (throughout the myocardial wall)

+ troponin

62
Q

Reperfusion injuries

A

increases cell injury through:

  1. Reactive oxygen species:
    ◊ Incomplete oxygen utilization by damaged mitochondria → reactive oxygen species (ROS) → damage to cell walls
  2. Inflammation:
    ◊ Inflammatory response produces cytokines → damage to cell walls
  3. Sarcoplasmic reticulum (normally regulates Ca++availability for contraction and relaxation) dysfunction:
    ◊ Sarcomere => the contractile unit of the myocyte
    ◊ IRI impairs the SR’s ability to recycle calcium (Ca2+ is continuously available)
    –Causing continual contraction (“Stunned” myocardium) and Cell wall damage
63
Q

Auscultation with ACS

A

S3 – suggestive of LV dysfunction
New onset MR – suggestive of papillary muscle dysfunction
New onset inspiratory crackles – suggestive of pulmonary congestion/LV dysfunction

64
Q

Troponin labs

A

To diagnose injury/necrosis

Results need to be contextualized with the patient since other conditions may cause false positives

Normal values:
□ cTnI: 0 - 0.04 ng/mL
□ hs-cTnI:
♀ < 16 ng/L
♂ < 34 ng/L

65
Q

Natriuretic peptide (BNP)

A

dx HF

66
Q

ACS workup

A

Presentation
H&P
Serial 12 leads
Labs (+ Serum markers)
Echo
Cardiac cath & coronary angiogram (time to table 90 min)

67
Q

HF definition

A

a clinical syndrome caused by a structural and/or functional cardiac abnormality and corroborated by elevated natriuretic peptide levels and/or objective evidence of pulmonary or systemic congestion

68
Q

HF risk factors

A

○ Increasing age
○ Pregnancy
○ Valvular heart disease
Esp. aortic stenosis
○ Myopathies – dilated (restrictive and hypertrophy)
○ Infections

69
Q

Forward and backward effects

A

Forward effects: Decreased cardiac output and stroke volume causes inadequate arterial tissue perfusion
□ Brain: AMS
□ Circulatory system: weak, thready pulses; tachycardia; hypotension
□ GI tract: nausea, anorexia, abd discomfort
□ Kidneys: decreased UOP, increased BUN/Cr, CKD
□ Skeletal muscle: weakness, chronic fatigue, exercise intolerance
□ Skin: cool, mottled, cyanotic

Backward effects: Decreased cardiac output and stroke volume causes left ventricular volume overload which is transmitted “backwards” to the pulmonary circulation (congestion) and eventually the venous circulation (edema)
□ Respiratory s/sx: tachypnea, hypoxemia, air hunger
□ Venous congestion: JVD, hepatomegaly

70
Q

EF calculation

A

EF= SV/EDV ×100

Example with normal values:
EF= (70 mLs)/(100 mLs ) ×100=70%

71
Q

HFrEF anatomical chx and manifestations

A

EF </= 40%

Myocardial walls thin and weak
Chamber dilates
End diastolic volume and pressure is high → ↓ SV

Myocytes exchanged for scar tissue and fibroblasts, surrounded by collagen

Cardiomegaly

S3 heart sound

72
Q

HFrEF co-morbidities & pathophys

A

Hypertension + atherosclerosis → coronary heart disease → acute coronary syndrome → myocardial injury/infarction → myocytes replaced with scar tissue (not contractile)

RAA and SNS contribute to abnormalities

73
Q

HFpEF anatomical chx and manifestations

A

EF >/= 50%

Myocardial hypertrophy and stiffness (non-compliant)
Remodeling and thickening
More densely packed collagen and fibroblasts around myocytes (fibrotic muscle)

Chamber volume small → ↓ SV

Tachycardia shortens diastolic filling time and exacerbates symptoms

S4 heart sounds

74
Q

HFpEF co-morbidities & pathophys

A

Aging + HTN + DM + aging + obesity + renal dysfunction
→ activation of inflammatory and fibrotic mechanisms
→ hypertrophy and LV remodeling
→ myocardial dysfunction
→ fibrosis, extracellular collagen excess

HIGH PRESSURE
LOW VOLUME

75
Q

DM effects on cardiomyocytes

A

ROS
Glucose toxicity
– Chronically elevated glucose levels increase AGEs and have a profibrotic change on the heart
—Primarily has a dominant effect on diastolic dysfunction

Advanced glycation end productions (AGES)
– Myocardium has receptors for advanced glycation end productions (RAGES)
– Increases ROS, oxidative stress, and inflammation
– Glycation: glucose attachment to Hgb

76
Q

S3 heart sound

A

Gallop

Passive atrial filling of an overfilled ventricle in early diastole yields an S3 heart sound (gallop)

The ventricle should be empty because of the previous stroke volume; however, it is overfull due to HF, so as atrial blood enters, it produces the S3 sound

77
Q

S4 heart sounds

A

Atrial contraction into non-compliant ventricles leads to an S4 heart sound

Blood at very end of diastole is from atrial contraction/kick

78
Q

Natriuretic peptide labs

A

B-type natriuretic peptides (BNP) and n-terminal pro B-type natriuretic peptide (NT-BNP)

Cells in the cardiac ventricles release NP in response to distension

Elevated values correlate to increased end diastolic volume

NPs trigger sodium triuretic (diuresis), which is an adaptive response (removes blood volume)

79
Q

AHA HF Stages

A

A: @ risk but NO structural disease or sx
B: Structural disease but NO sx
C: Structural disease WITH sx (prior or current)
D: Refractory HF requiring specialized interventions

80
Q

NYHA functional classifications

A

I: No limitations or sx
II: Slight limitations and sx with ordinary activity
III: Marked limitations and sx with less than ordinary activity
IV: Sx at rest or inability to perform any physical activity

81
Q

Universal definition of HF classification by EF

A

HFrEF <40%
HFmrEF (mildly reduced) 41-49%
HFpEF >50%
HFimpEF (improved) 10 point increase from BL (<40%) and a second measurement >40%

82
Q

RV HF

A

Pulmonary vessels constrict in response to disease

Increased PVR and afterload on RV

Problems with gas exchange (hypoxemia)

83
Q

High output HF

A

Heart is normal (sufficient blood volume and contractility), yet cannot meet the oxygen needs of the body

Excessive tissue oxygen demands –> tissue hypoxia –> catecholamines –> increased HR and SV –> increased CO

The hyperdynamic heart cannot keep up with the O2 demands –> tissue hypoperfusion –> ischemia/injury/ necrosis + metabolic (lactic) acidosis

84
Q

HF in sepsis

A

Causes a release of histamines and leukotrienes
—Cause gross vasodilation of blood vessels
◊ SVR decreases (arterial resistance), thus reducing afterload
— Bacteria (esp. gram -) release toxins that prevent cells from uptaking O2

Increased CO, but heart cannot keep up with demands

Advanced Pathophysiology (6 decks)

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