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DTC 330: Medical Nutrition Therapy > CardioVascular > Flashcards

CardioVascular Flashcards

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USMLE® Step 1 flashcards
1
Q

Arteries

A

carry blood away from heart

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2
Q

Veins

A

Carry blood towards the heart

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3
Q

Capillaries

A

Where nutrients and gases exchange occur

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4
Q

Functions of the cardio system?

A 
Regulates blood flow to tissues
Retrieves waste products
Thermoregulation
Gas exchange
Closed loop of blood vessels
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5
Q

Blood flow pattern??

A
  1. 02 poor blood returns via inferior and superior vena
  2. R atrium
  3. R ventricle
  4. LR Pulmonary
  5. Lungs
  6. Co2 removed and O2 added
  7. Blood returns
  8. Heart via LR pulmonary vein
  9. L atrium
  10. L ventricle
  11. Pumped to the systemic circulation through aorta
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6
Q

SA node?

A 
Sinoatrial node (Pacemaker)
Initiates heartbeat and causes atria to contract on average 0.85 seconds
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7
Q

Systole?

A

Contraction of the heart chambers

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8
Q

Diastole?

A

Relaxation of the heart chambers

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9
Q

Stroke volume?

A

Volume of blood ejected with each contraction of the L ventricle with each systolic phase

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10
Q

Ejection Fraction (EF):

A

Fraction of blood that is ejected from heart by contraction of left ventricle.

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11
Q

Mean arterial BP(MAP):

A

determined by a combo of cardiac output and total peripheral resistance

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12
Q

Normal range BP:

A

70-110 mm Hg to perfuse all organs, tissues

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13
Q

Regulation of MAP:

A

Sympathetic nervous system
Renin-angiotensin system
The role of kidney in BP regulation

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14
Q

Kidneys role in RAAS

A

Kidneys secrete peptide hormone renin in response to reduced NaCl, ECF volume, and arterial BP.
Renin activates angiotensinogen

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15
Q

What is angiotensinogen?

A

plasma protein produced by the liver

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16
Q

Conversation of angiotensinogen

A

Angio 1 to angio 2 by ACE (angiotensin-converting enzyme) produced by lungs.
Ang 2 stimulates the adrenal cortex to secrete hormone aldosterone which stimulates Na reabsorption by kidneys. Resulting retention of Na exerts osmotic effect that holds more h20 in ECF.

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17
Q

Vasopressin?

A

Antidiuretic hormone
known as Arginin Vasopressim (AVP)
Secreted from posterior pituitary gland in response to increased plasma osmolality. Results in concentration of urine and reduced urine volume

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18
Q

Hypertension

A

Defined as chronic elevation in BP > 140/90 mmHg

Silent killer damages heart and arteries

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19
Q

Etiology of HTN

A

Primary or essential idiopathic- no known causes 90% of all cases
Age, ethnicity, family history. high BW
Secondary- results of another chronic condition: Renal, cvd, endocrine disorders, or neurogenic disorders.
Lifestyle factors- smoking, exercise, diet, sodium intake

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20
Q

Pathophysiology of HTN?

A

Excessive secretion of Vasopressin and angio2-increase BP
Smoking
Renal disease: interferes with action of nitric oxide, impairs endothelial relation and vasodilation
Adrenal disorders: excessive secretion of epinpherine and norepinephrine
Neurological disease: affecting medulla oblangata

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21
Q

Treatment of HTN?

A

Reduce risk of CVD and renal disease
Lower BP < 140/90
Weigh reduction, physical activity, nutrition therapy, pharmocological intervention

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22
Q

Medical treatment for HTN?

A
  1. Loop diuretics: Acted by inhibiting Na, Cl, K reabsorption in loop of henle of kidney
  2. Thiazides: same action as loop but in distal tubule and ascending loop of henle
  3. Carbonic anhydrase inhibitors: block enzyme involved with exchange of H+ with Na and H20.
  4. Potassium sparing diuretics: acts within the collecting and convoluted tubes- prevent sodium-potassium exchange and reduce aldosterone stimulation
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23
Q

Lasix

A

Lasix (furosemide) is a loop diuretic (water pill) that prevents your body from absorbing too much salt. This allows the salt to instead be passed in your urine.

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24
Q

DASH diet?

A 
Dietary Approaches to Stop Hypertension
4-5 servings of Fruit
4-5 servings of vegetables
2-3 servings of nonfat, low fat dairy
6-8 servings of whole grains
2 or less servings of meat, poultry, or fish
Nuts, seeds, and dry beans- 4/5 week
Decrease total and sat fat
Decrease sodium: 1500-2400mg/d
Increase Ca, K, and Mg
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25
Q

Core of Lipoprotein

A

TG and Cholesterol esters

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26
Q

Lipoprotein surface?

A

Phospholipids
Proteins
Cholesterol

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27
Q

LDL is made up of what?

A

Mostly free cholesterol

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28
Q

Atheroscelrosis

A

Thickening of blood vessel walls caused by presence of plaque (AS) “hardening”

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29
Q

Arterioscelerosis

A

more general term includes loss of vascular elasticity- results in restriction of blood flow

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30
Q

Plaque development?

A

Renin-angiotensin system plays a role, tobacco, oxidized LDL, glycated substances from DM, and homocysteine.

31
Q

What does nitric oxide have to do with atheroscelrosis?

A

An imbalance of NO is caused by oxidative stress, and NO contributes towards endothelial control like normal relaxation of smooth muscle in arteries, regulates leukocyte adhesion, platelet adhesion, and thrombosis.

32
Q

Foam cells?

A

filled with cholesterol and are released into EX spaces where they form fatty streaks. This streak can occur as early as age 5

33
Q

Thrombus

A

blood clot that stays

34
Q

Embolus

A

blood clot that breaks from cellular surface and freely moves through the circulation.

35
Q

Pathophysiology of Athersclerosis

A 
Inflammatory response
Injury to endothelial lining
Attracts platelets
Forms small clots
Continued migration of cells to area
Proliferation of the plaque
Rupture of fibrous cap can occur
36
Q

Gynoid obesity?

A

Fat around the hips

37
Q

Android?

A

Fat around abdominal fat and insulin resistance, have a higher waist circumference which is assoc with risk of CVD

38
Q

Diagnosing criteria for Metabolic Syndrome

A 
Any 3 of the 5 constitutes MS
Waist circumference
TG
HDL
BP 
and Fasting Glucose
39
Q

Desirable Lab Values

A

Total Cholesterol: <200 mg/dL
HDL >60mg/dL
LDL: <100mg/dL
TG: <150mg/dL

40
Q

TLC Diet

A 
Sat fat: <7%
PUFA: up to 10%
MUFA: Up to 20%
Total F: 25-35% of kcal
Chol: <200 mg/day
Carb: 50-60% kcal
Fiber: 20-30g/day
Pro: Approx 15% of kcal
Na: 2400 mg/day
Stanol esters: 3.4g
41
Q

Plant sterols?

A

Naturally occuring component of plant membranes just as cholesterol (animal).
Most abundant:
Beta-sitosterol
Campesterol
Stigmasterol
Structurally resemble cholesterol, not synthesized by humans.
Lowers serum cholesterol by inhibiting absorp of dietary and biliary cholesterol

42
Q

Foods bearing claim must contain:

A
  1. 65g of plant sterols per serving

1. 7g of stanol esters per serving

43
Q

Ischemia:

A

local temporary reduced blood supply d/t obstruction of heart “restriction”

44
Q

Soft lipid?

A

more likely to cause MI
less likely to occlude large areas within the lumen
More prone to rupture
have a fibrous cap covering lipid rich core with macrophages
Inflammation from within the plaque will weaken the cap
Macrophages secrete substances that weaken cap

45
Q

Large hardended plaques

A 
Have more smooth muscle cells
Less likely to rupture
May occlude up to 70% of artery
May cause angina
Collateral circulation may develop over time
will occlude the artery without infarct
46
Q

Occlusion

A

Narrowing of the coronary artery from the buildup of cholesterol. This buildup is known as plaque in arteries throughout the body is called atheroscelrosis

47
Q

Angina

A

Condition when a pt complains of chest pain due to lack of blood supply
Happens slowly with warning signs
Sudden blockage of vessel d/t acute plaque rupture and closure of artery w/ clot buildup

48
Q

Stable angina

A

sub sternal pain when workload is increased, physical or emotional stress

49
Q

Unstable angina

A

rapidly worsening chest pain on minimal exertion or at rest

50
Q

MI and angina initiated by:

A 
Sudden blockage
Hemorrhage
Arterial spasm
Increase in myocardial oxygen demand
One common factor:
occlusion of lumen by AS plaque
51
Q

Infarction:

A

area of dead tissue d/t loss of blood supply- resulting in development of necrotic tissue

52
Q

What are the biomarkers for dx in MI?

A

Levels increase in blood then return to normal
CK-MB: more specific for cardiac tissue
CK: Creatine kinase
M and B: 2 polypeptides and form an isoenzyme of creatine kinase
Lactate dehydrogenase isoenzyme (LD-I)
cTnT and cTnI: Cardiac troponin T and I

53
Q

What are cardiac biomarkers?

A

protein molecules released into blood stream from damaged heart muscle
Characteristic rise and fall pattern

54
Q

Creatine kinase:

A

Increased in over 90% of MI, can also be increased in muscle trauma, physical exertion, post-op, convulsions

55
Q

LDH-I

A 
Predominates in heart and red cells
Increases later than CK 
Normal levels; 313-618U/L
Reaches max level in 48-72h
Remains elevated for 7-10 days after MI
56
Q

Troponin T and I

A

protein complex located on thin filament of striated muscles and are used as biomarkers for MI dx
Cardiac troponins different than skeletal muscle.
Isoforms very specific to cardiac injury
Preferred markers
Normal levels: 0.5ng/dL
Rise 4-6 hours, peak 12 hours, and return to normal 3-10 days

57
Q

Post-MI Nutrition Therapy?

A

Reduce oral intake d/t pain, anxiety, fatigue, SOB
Limit intake to clear liquids
No caffeine to prevent arrhythmias, and decrease risk of vomiting and aspiration
Progress to soft, easily chewable foods
Small freq meals
Reduce exertion
Follow ATP III guidelines

58
Q

The primary target of therapy

A

LDL Cholesterol

59
Q

Stroke?

A 
Sudden brain damage b/c lack of blood flow to the brain caused by a clot or rupture of a blood vessel
Embolic: travels to the brain
Thrombotic: Clot develops in artery
Hemorrhagic= bleed
Bleeindg around brain and into blain
60
Q

Peripheral artery disease (PAD)

A

Occlusion of blood flow in non-coronary arteries (lower extremities)
Similar to AS and IHD
Eventually suffer from denervation of affected muscle
Can cause ulceration; commonly foot or toes.

61
Q

Claudication

A

fatigue- heaviness, tiredness, cramping in the leg,

Pain or discomfort goes away once the activity is stopped or during rest.

62
Q

Heart failure-

A

Impairement of ventricles capacity to eject or fill with blood
underlying cause- structural or functional
End stage CVD

63
Q

Stages of Heat Disease

A

A: at risk but no structural abnormalities
B: Have structural disease but demonstrate no symptoms of HF
C: Patients w/ past or current symptoms of HF who have underlying structural HD
D: Patients with end-stage disease req specialized treatment, mech circulatory support, procedures to facilitate fluid removal.

64
Q

Dyspnea

A

shortness of breath (SOB)

65
Q

Orthopnea

A

SOB of breath associated with lying in supine position

66
Q

Cardiac cachexia

A

Unintended weight loss due to cardiac complications

67
Q

Left-sided failure

A

includes dyspnea and orthopnea

68
Q

Right-sided failure

A

fluid retention

pulmonary congestion, edema, hepatomegaly, splenomegaly, ascites.

69
Q

Nutrition therapy for CHF

A 
50% of HF failure patients are malnourished
Increased workload/difficulty eating
Goal decrease work of heart
2g sodium is standard
fluid restriction 1mL/kcal or 35mL/kg
Alcohol non to mod
Caffeine can cause MI or cardiac arrhythmia
Fluid restricting EN formula if needed
70
Q

Arginine

A

for increased production of NO

71
Q

Carnitine:

A

ships FA into mitochondria for oxidation

72
Q

Taurine:

A

reduced BP and combined with carnitine alleviates muscle fatigue in strenous workouts and raises exercise capacity

73
Q

Factors assoc with development of cardiac cachex

A 
Generalized cellular hypoxia
Decreased energy intake
Anorexia secondary to ascites with drug therapy
Unpalatable diet and fluid restriction
Breathlessness and exhaustion from eating
Altered taste and smell
Depression
N/V
74
Q

Heart transplant phases

A

Pre-transplant: control kcal, pro, Na, K, Fat, Chol
Avoid fluid overload

Immediate post: increase diet as tolerated
Follow DASH diet plan, Omega-3 FA, Vit Supp

Long-term post: Continue with education/monitoring

DTC 330: Medical Nutrition Therapy (5 decks)

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