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Health Studies > MI Roop/Reza > Flashcards

MI Roop/Reza Flashcards

1
Q

A 66-year-old woman presents to the ED with a CC of shortness of breath and chest pain that extends to her neck. She states that she has had difficulty sleeping for the past few nights and states she is more tired than usual. She is a retired administrative assistant who smokes one pack of cigarettes a day and drinks alcohol socially. Her BMI is 33 and she has been taking captopril to control her b.p. What type of BP medication is captopril?

A

ACE inhibitor

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2
Q

A 66-year-old woman presents to the ED with a CC of shortness of breath and chest pain that extends to her neck. She states that she has had difficulty sleeping for the past few nights and states she is more tired than usual. She is a retired administrative assistant who smokes one pack of cigarettes a day and drinks alcohol socially. Her BMI is 33 (obese) and she has been taking captopril (ACE inhibitor) to control her b.p. Pt. states she ran out of captopril two weeks ago and never refilled her prescription. Vital signs: Temp. = 98.6◦F, Pulse = 88/min, Resp. = 23/min, BP = 150/105 mmHg. Physical exam showed pale and diaphoretic (sweating), neurologic exam is normal, pt. very anxious. What is causing these signs and symptoms? What test should be run next?

A

-Sympathetic NS working in overdrive
-ECG/EKG should be done next

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3
Q

ECG is a wide ___ wave in leads I and aVL (a= augmented)

A

Q

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4
Q

An EKG lead consists of two surface electrodes of opposite polarity (one positive and one negative) or one positive surface electrode and a reference point. A lead composed of two electrodes of opposite polarity is called a __________ lead. A lead composed of a single positive electrode and a reference point is a ____________ lead.

A

bipolar, unipolar

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5
Q

For a routine analysis of the heart’s electrical activity an ECG recorded from 12 separate leads is used. A 12-lead ECG consists of three bipolar limb leads (I, II, and III), the unipolar limb leads (AVR, AVL, and AVF), and _____ unipolar chest leads, also called precordial or V leads.

A

6

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6
Q

A 12 point ECG allows you to get a 3D look at the heart and pinpoint any deficit in….

A

conduction

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7
Q

A 66-year-old woman presents to the ED with a CC of shortness of breath and chest pain that extends to her neck. She states that she has had difficulty sleeping for the past few nights and states she is more tired than usual. She is a retired administrative assistant who smokes one pack of cigarettes a day and drinks alcohol socially. Her BMI is 33 (obese) and she has been taking captopril (ACE inhibitor) to control her b.p. Pt. states she ran out of captopril two weeks ago and never refilled her prescription. Vital signs: Temp. = 98.6◦F, Pulse = 88/min, Resp. = 23/min, BP = 150/105 mmHg. Physical exam showed pale and diaphoretic (sweating), neurologic exam is normal, pt. very anxious. Lab studies show ST segment elevation in leads I, aVL and V2-5, blood tests: elevated troponin & CK-MB, lipid panel: cholesterol high, HDL low & LDL high. What is the diagnosis?

A

-MI caused by coronary artery disease (CAD)
-Most likely happened a couple days ago because she had trouble sleeping and enzymes are still elevated

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8
Q

What does P wave indicate?

A

atrial depolarization, atrial contraction happens after

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9
Q

What is QRS?

A

ventricular depolarization

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10
Q

What is the T wave?

A

ventricular repolarization

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11
Q

What is happening in the ST segment?

A

-Ventricular contraction
-Should be electrically neutral/ a flat line
-ST elevation → something is wrong with heart tissue

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12
Q

A 66-year-old woman presents to the ED with a CC of shortness of breath and chest pain that extends to her neck. She states that she has had difficulty sleeping for the past few nights and states she is more tired than usual. She is a retired administrative assistant who smokes one pack of cigarettes a day and drinks alcohol socially. Her BMI is 33 (obese) and she has been taking captopril (ACE inhibitor) to control her b.p. Pt. states she ran out of captopril two weeks ago and never refilled her prescription. Vital signs: Temp. = 98.6◦F, Pulse = 88/min, Resp. = 23/min, BP = 150/105 mmHg. Physical exam showed pale and diaphoretic (sweating), neurologic exam is normal, pt. very anxious. Lab studies show ST segment elevation in leads I, aVL and V2-5, blood tests: elevated troponin & CK-MB, lipid panel: cholesterol high, HDL low & LDL high. What do a wide Q wave and deviations on the ST segment primarily indicate?

A

-Wide QRS cannot see V-fib on ECG
-Wide QRS = ventricular tachycardia
-Wide Q wave = MI
-With the ECG you could think:
»Tissue being damaged (ischemia, MI)
»Blockage in coronary vessel

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13
Q

How much oxygen does the heart tissue extract from coronary vessels?

A

-95% (more than any other tissue in the body, regular tissues will be 40% or less)
-Cardiac metabolism and blood flow through the heart must be matched (normally)

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14
Q

R/L coronary artery branches from the ___________________ (base) running in the coronary sulcus

A

ascending aorta

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15
Q

Right coronary artery branches into the…

A

posterior IV artery and right marginal artery

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16
Q

Left coronary artery branches into the…

A

LAD artery, left marginal artery, and circumflex artery

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17
Q

What is ischemia?

A

-Blood flow and cardiac metabolism are not matched
-Can cause necrosis and result in MI

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18
Q

2 types of deviations in ST segments (for acute MI)

1) non-ST-segment-elevation MI (NSTEMI)

2) ST-segment-elevation MI (STEMI, also known as transmural MI)
-Myocardial necrosis w/ ECG changes showing ST segment elevation that is not quickly reversed by ___________
-Troponin I or troponin T and Ck are elevated
-Case study patient had STEMI

A

nitroglycerin

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19
Q

What does Transmural MI mean?

A

all three layers of the heart are affected

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20
Q

Troponin appears in the plasma soon after damage and indicates ____________- most specific and most sensitive of the serum markers

A

infarction

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21
Q

CK-MB- creatine kinase myocardial band appears __ hours after injury and peaks at about ______ hours

A

4, 24

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22
Q

A 66-year-old woman presents to the ED with a CC of shortness of breath and chest pain that extends to her neck. She states that she has had difficulty sleeping for the past few nights and states she is more tired than usual. She is a retired administrative assistant who smokes one pack of cigarettes a day and drinks alcohol socially. Her BMI is 33 (obese) and she has been taking captopril (ACE inhibitor) to control her b.p. Pt. states she ran out of captopril two weeks ago and never refilled her prescription. Vital signs: Temp. = 98.6◦F, Pulse = 88/min, Resp. = 23/min, BP = 150/105 mmHg. Physical exam showed pale and diaphoretic (sweating), neurologic exam is normal, pt. very anxious. Lab studies show ST segment elevation in leads I, aVL and V2-5, blood tests: elevated troponin & CK-MB, lipid panel: cholesterol high, HDL low & LDL high. What can be assumed with the cardiac markers?

A

Both troponin and CK-MB are elevated so it can be assumed that she had an MI at least one day prior

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23
Q

A 66-year-old woman presents to the ED with a CC of shortness of breath and chest pain that extends to her neck. She states that she has had difficulty sleeping for the past few nights and states she is more tired than usual. She is a retired administrative assistant who smokes one pack of cigarettes a day and drinks alcohol socially. Her BMI is 33 (obese) and she has been taking captopril (ACE inhibitor) to control her b.p. Pt. states she ran out of captopril two weeks ago and never refilled her prescription. Vital signs: Temp. = 98.6◦F, Pulse = 88/min, Resp. = 23/min, BP = 150/105 mmHg. Physical exam showed pale and diaphoretic (sweating), neurologic exam is normal, pt. very anxious. Lab studies show ST segment elevation in leads I, aVL and V2-5, blood tests: elevated troponin & CK-MB, lipid panel: cholesterol high, HDL low & LDL high. What would make you think that this patient had atherosclerosis?

A

-High LDL
-Pain
-HTN
-Obese (BMI)
-Smoking

24
Q

What is the progression of atherosclerosis?

A

1) Normal
2) Endothelial dysfunction
3) Fatty streak formation
4) Stable (fibrosis) plaque formation
-Fibrous cap is stable and will most likely not rupture
-Decreasing lumen blood flow
-Intermittent claudication, angina, etc.
5) Unstable plaque formation
-fibrous cap is thin and can rupture at anytime and become embolism (thrombus = stays, embolism = moves)
-MMP (matrix metalloproteinases) destroys the collagen of the fibrous cap
-Case study patient most likely had unstable plaque and no blood flow going through coronary arteries

25
Q

What is happening in this diagram?

A

→ injury to endothelium triggers monocyte adhesion
→ loosening of endothelial cell junctions
→ migration of monocytes beneath endothelium
→ monocytes differentiate into macrophages
→ more permeable endothelium permits LDL to enter intima of artery
→ macrophages begin engulfing LDL by phagocytosis
→ macrophages become filled w lipids from ingesting LDL
→ macrophages now referred to as “foam cells”
→ collections of foam cells create fatty streaks

26
Q

What are the symptoms of MI? Are there differences between men and women? How are they similar?

A

Women
-Indigestion
-feel acid reflux
-abdominal pain
-upper back pain (between shoulders)
-chest pain → usually localized to area
-Something that doctors usually misses in women is fatigue

Men
-severe, steady, chest pain that radiates to left arm neck and jaw
-Sweating

both
-Fever
-Pallor
-dyspnea
-Anxiety
-Hypotension
-SOB

27
Q

What are the risk factors for coronary heart disease? Did the case study patient have any? If so, what are they?

A

-High cholesterol (case study pt)
-Smoking (case study pt)
-Not taking medications (had previous HTN) (case study pt)
-Diet (case study pt)
-Age (case study pt)
-Lack of exercise (case study pt)
-Menopause (case study pt)
-Family history
-Sex (men are more likely)
-Diabetes
-Drinking

28
Q

What does the histology look like for acute MI?

A

-Yellow necrosis with blood around the borders (hyperemic)
-Hypereosinophilia
-Transmural, ruptured left ventricular wall (eosinophils + neutrophils infiltration bc tissue is dying)
-Neutrophil infiltration

29
Q

Pain stimulates the sympathetic NS. How is this reflected in the case study patient’s S&S?

A

-Anxious
-Increased BP (increases workload on the L ventricle)
-Increased HR (decreased duration of diastole decreases blood flow into L ventricle)
-Increases ventricular contractility (increased workload)
-High respiratory rate, sweating

30
Q

Pain stimulates the sympathetic NS. The 1st purpose of treatment is to try to restore _________.

A

oxygen

31
Q

What are the treatment options for acute MI

A

-Supplemental oxygen to oxygenate arterial blood
-Nitroglycerin to vasodilate (nitroglycerin breaks down into NO and vasodilates all the arteries in the area)
-Aspirin- cyclooxygenase inhibitor to decrease possibility of platelet plugs
-Clot-dissolving med if doctor suspects that there is a thrombus, give pt tPA (tissue plasminogen activator) which greatest efficacy is given within first hour of the episode, but has 2 hr window for heart

32
Q

What is the MOA of aspirin?

A

Irreversible inhibition of cyclooxygenase enzyme via acetylation

Small dose (75-325 mg/dl) inhibits thromboxane synthesis in platelets (TXA2) but not prostacyclin (PGI2) synthesis in endothelium (larger dose > 1000 mg)

33
Q

tPA is a fibrinolytic drug that induces successful recanalization of occluded blood vessels while making sure that the surrounding region is….

A

viable

34
Q

What is the MOA of tPA?

A

Breaks down blood clots via conversion of plasminogen to plasmin

35
Q

tPA activity is regulated by _____________, which increases its catalytic efficiency (unlike uPA, other plasminogen activator)

A

fibrin-binding

36
Q

Pain stimulates the sympathetic NS. To decrease pain, the pt is usually given ____________ to decrease the effects of the activation of the sympathetic NS

A

morphine

37
Q

What are the surgical treatment options for MI?

A

-Cardiac catheterization (stent)
-Coronary artery bypass graft surgery (CABG)

38
Q

Explain the ATP production process in heart tissue.

A

-Under physiological conditions, >90% of ATP produced in the cardiac monocytes is supplied by mitochondria via oxidative phosphorylation (OXPHOS), and the remainder comes from glycolysis and GTP derived from the TCA cycle
-The majority of cardiac ATP is consumed by the myofilaments, and 25% of cardiac ATP hydrolysis is used to fuel ion channels and transporters

39
Q

Under what conditions does acidosis occur in heart tissue?

A

During MI or metabolic inhibition, various metabolic parameters are markedly altered in cardiac myocytes
-ATP levels decrease, cells become progressively acidic with elevated lactate levels, and the levels of phosphate and magnesium increase

40
Q

How are fatty acids metabolized?

A

Fatty acids are broken down to acetyl-CoA by means of beta oxidation inside the mitochondria

41
Q

How does diabetes affect the cellular mechanism causing heart failure?

A

-One of the main contributors to the accelerated cardiac fatty acids flux rates in diabetes is the increase in circulating free fatty acids
-Augmented levels of circulating free fatty acids are partly due to the fact of insulin resistance in the adipose tissue, which increases lipolysis and circulating fatty acids
-Genetic deficiencies in carnitine palmitoyltransferase 2 (CPT 2) expression, particularly in the cardiac and skeletal muscle can lead to cardiomyopathy and myoglobinuria following prolonged exercise
-In the diabetic heart, ATP production becomes almost completely reliant on FA oxidation
»ATP wasting

42
Q

What are potential treatments for heart failure? In regards to ROS, glycolysis and FAO.

A

Beta blockers
-Target cardiac metabolism by inhibition of CPT2 activity. This results in increased glucose oxidation and more efficient oxygen use for ATP production
-Can inhibit FA oxidation, which may be beneficial in failing heart as its shifting from FA oxidation to glucose oxidation is more oxygen efficient

ACE inhibitors and angiotensin receptor blockers
-Ang 1 is converted to Ang 2 by ACE
-Ang 2 damages mitochondria in the failing heart through generation of ROS
-Ang 2 likely reduces glucose oxidation, acetyl coa, and ATP by upregulating PDK expression

Sodium glucose transport protein 2 (SGLT2) inhibitors
-Pts w/ DM type 2 and HF can benefit from these inhibitors
-SGLT2 inhibitors improve cardiac function by increasing ketones, free FAs, and BCAA

Inhibition of long chain 3-ketoacyl thiolase CoA shifts myocardial metabolism from FA oxidation to glucose oxidation

Malonyl CoA decarboxylase (MCD) inhibitors
-Increases cardiac malonyl CoA levels
-Causes inhibition of CPT2, which results in reduced mitochondrial FA reuptake and favoring of glucose oxidation pathways

43
Q

A 32-year-old man presents to the ED with CC of postprandial chest pain. What is postprandial chest pain?

A

Pain after eating

44
Q

A 32-year-old man presents to the ED with CC of postprandial chest pain. Pt. had eaten pizza several hours previously. One hour after consumption he experienced pain, described as, ‘crushing’; nausea, diaphoresis and dyspnea. He rated the pain as 7/10 but admitted it did not worsen with respiration, nor did it radiate. No significant med hx. Pt takes no meds, allergic to PCN. Father had an MI at 51 years of age. Lives with his girlfriend who is recovering from a Strep. Pharyngitis. Pt is under a lot of stress as he just started a new job, moved to a new apartment and recently lost a much loved pet. Pt drinks a six-pack of beer daily and uses cocaine occasionally – most recently three months ago. Vital signs show temp. = 97.3◦F, pulse = 83/min, BP = 158/81 mmHg, resp. = 28/min, oxygen sat. = 100%. Physical exam shows BMI = 26.9, pt. is anxious and diaphoretic (sweating), negative for heart murmur, pt points to subxiphoid area (below sternum) as the main site of pain & there is tenderness upon palpation. Lab studies show urine w/ presence of cannabinoids, Hct = 40.6% (slightly low), Cl = 98 mmol/L (normal), Glucose = 123 mg/dL (high), AST = 42 (high), Troponin T < 0.03 (normal), ECG: ST-segment elevation, PR- segment elevation, Chest x-ray: negative for pneumothorax or cardiomegaly. Lungs clear. The initial treatment was ASA (aspirin) and clopidogrel (plavix, blood thinner), but there was no change in pain. Could this be pericarditis? Why or why not?

A

-Potentially
-If yes, could be from girlfriend’s infection
-If no, could be bc he came in having pain upon eating
»Pain for pericarditis = in the center

45
Q

A 32-year-old man presents to the ED with CC of postprandial chest pain. Pt. had eaten pizza several hours previously. One hour after consumption he experienced pain, described as, ‘crushing’; nausea, diaphoresis and dyspnea. He rated the pain as 7/10 but admitted it did not worsen with respiration, nor did it radiate. No significant med hx. Pt takes no meds, allergic to PCN. Father had an MI at 51 years of age. Lives with his girlfriend who is recovering from a Strep. Pharyngitis. Pt is under a lot of stress as he just started a new job, moved to a new apartment and recently lost a much loved pet. Pt drinks a six-pack of beer daily and uses cocaine occasionally – most recently three months ago. Vital signs show temp. = 97.3◦F, pulse = 83/min, BP = 158/81 mmHg, resp. = 28/min, oxygen sat. = 100%. Physical exam shows BMI = 26.9, pt. is anxious and diaphoretic (sweating), negative for heart murmur, pt points to subxiphoid area (below sternum) as the main site of pain & there is tenderness upon palpation. Lab studies show urine w/ presence of cannabinoids, Hct = 40.6% (slightly low), Cl = 98 mmol/L (normal), Glucose = 123 mg/dL (high), AST = 42 (high), Troponin T < 0.03 (normal), ECG: ST-segment elevation, PR- segment elevation, Chest x-ray: negative for pneumothorax or cardiomegaly. Lungs clear. The initial treatment was ASA (aspirin) and clopidogrel (plavix, blood thinner), but there was no change in pain. Could this be cardiac ischemia?

A

-Potentially
-If yes, its bc aspirin did not help and cardiac ischemia could be due to HTN
-If no, its bc troponin levels were normal, pt had pain after eating in subxiphoid process and had 100% oxygen levels

46
Q

A 32-year-old man presents to the ED with CC of postprandial chest pain. Pt. had eaten pizza several hours previously. One hour after consumption he experienced pain, described as, ‘crushing’; nausea, diaphoresis and dyspnea. He rated the pain as 7/10 but admitted it did not worsen with respiration, nor did it radiate. No significant med hx. Pt takes no meds, allergic to PCN. Father had an MI at 51 years of age. Lives with his girlfriend who is recovering from a Strep. Pharyngitis. Pt is under a lot of stress as he just started a new job, moved to a new apartment and recently lost a much loved pet. Pt drinks a six-pack of beer daily and uses cocaine occasionally – most recently three months ago. Vital signs show temp. = 97.3◦F, pulse = 83/min, BP = 158/81 mmHg, resp. = 28/min, oxygen sat. = 100%. Physical exam shows BMI = 26.9, pt. is anxious and diaphoretic (sweating), negative for heart murmur, pt points to subxiphoid area (below sternum) as the main site of pain & there is tenderness upon palpation. Lab studies show urine w/ presence of cannabinoids, Hct = 40.6% (slightly low), Cl = 98 mmol/L (normal), Glucose = 123 mg/dL (high), AST = 42 (high), Troponin T < 0.03 (normal), ECG: ST-segment elevation, PR- segment elevation, Chest x-ray: negative for pneumothorax or cardiomegaly. Lungs clear. The initial treatment was ASA (aspirin) and clopidogrel (plavix, blood thinner), but there was no change in pain. Could the pain be non-cardiac in origin? Give examples

A

-GERD
-Diverticulitis
-Hernia
-Peptic ulcers
-Musculoskeletal

47
Q

A 32-year-old man presents to the ED with CC of postprandial chest pain. Pt. had eaten pizza several hours previously. One hour after consumption he experienced pain, described as, ‘crushing’; nausea, diaphoresis and dyspnea. He rated the pain as 7/10 but admitted it did not worsen with respiration, nor did it radiate. No significant med hx. Pt takes no meds, allergic to PCN. Father had an MI at 51 years of age. Lives with his girlfriend who is recovering from a Strep. Pharyngitis. Pt is under a lot of stress as he just started a new job, moved to a new apartment and recently lost a much loved pet. Pt drinks a six-pack of beer daily and uses cocaine occasionally – most recently three months ago. Vital signs show temp. = 97.3◦F, pulse = 83/min, BP = 158/81 mmHg, resp. = 28/min, oxygen sat. = 100%. Physical exam shows BMI = 26.9, pt. is anxious and diaphoretic (sweating), negative for heart murmur, pt points to subxiphoid area (below sternum) as the main site of pain & there is tenderness upon palpation. Lab studies show urine w/ presence of cannabinoids, Hct = 40.6% (slightly low), Cl = 98 mmol/L (normal), Glucose = 123 mg/dL (high), AST = 42 (high), Troponin T < 0.03 (normal), ECG: ST-segment elevation, PR- segment elevation, Chest x-ray: negative for pneumothorax or cardiomegaly. Lungs clear. The initial treatment was ASA (aspirin) and clopidogrel (plavix, blood thinner), but there was no change in pain. The pt received an invasive coronary angiography and was found to have normal epicardial coronary arteries and no L ventricular wall abnormalities. Pt. then stated that pain had subsided but now he had pain in the right upper quadrant, including upon palpation. Three hours later there was scleral icterus (yellow around the eyes) and dark-colored urine. Lab studies were done 7 hours later: Hg = 12.1 g/dL (slightly low), Hct = 34.1% (slightly low), platelet = 148,000 (slightly low), AST =196 (VERY HIGH), ALT = 284 (VERY HIGH), Total bilirubin = 5 mg/dL (VERY HIGH), Direct bilirubin = 2.6 mg/dL (VERY HIGH), Troponin <0.01 (normal, less than previous labs). What tests would you order now?

A

Ultrasound and scans

48
Q

A 32-year-old man presents to the ED with CC of postprandial chest pain. Pt. had eaten pizza several hours previously. One hour after consumption he experienced pain, described as, ‘crushing’; nausea, diaphoresis and dyspnea. He rated the pain as 7/10 but admitted it did not worsen with respiration, nor did it radiate. No significant med hx. Pt takes no meds, allergic to PCN. Father had an MI at 51 years of age. Lives with his girlfriend who is recovering from a Strep. Pharyngitis. Pt is under a lot of stress as he just started a new job, moved to a new apartment and recently lost a much loved pet. Pt drinks a six-pack of beer daily and uses cocaine occasionally – most recently three months ago. Vital signs show temp. = 97.3◦F, pulse = 83/min, BP = 158/81 mmHg, resp. = 28/min, oxygen sat. = 100%. Physical exam shows BMI = 26.9, pt. is anxious and diaphoretic (sweating), negative for heart murmur, pt points to subxiphoid area (below sternum) as the main site of pain & there is tenderness upon palpation. Lab studies show urine w/ presence of cannabinoids, Hct = 40.6% (slightly low), Cl = 98 mmol/L (normal), Glucose = 123 mg/dL (high), AST = 42 (high), Troponin T < 0.03 (normal), ECG: ST-segment elevation, PR- segment elevation, Chest x-ray: negative for pneumothorax or cardiomegaly. Lungs clear. The initial treatment was ASA (aspirin) and clopidogrel (plavix, blood thinner), but there was no change in pain. The pt received an invasive coronary angiography and was found to have normal epicardial coronary arteries and no L ventricular wall abnormalities. Pt. then stated that pain had subsided but now he had pain in the right upper quadrant, including upon palpation. Three hours later there was scleral icterus (yellow around the eyes) and dark-colored urine. Lab studies were done 7 hours later: Hg = 12.1 g/dL (slightly low), Hct = 34.1% (slightly low), platelet = 148,000 (slightly low), AST =196 (VERY HIGH), ALT = 284 (VERY HIGH), Total bilirubin = 5 mg/dL (VERY HIGH), Direct bilirubin = 2.6 mg/dL (VERY HIGH), Troponin <0.01 (normal, less than previous labs). An abdominal ultrasound was done and found to have gallstones in the gallbladder with a thick wall. The decision was made to remove the gallbladder as there was a high probability of cholecystitis along with the cholelithiasis.Surgery revealed a gallbladder filled with gallstones and a thickened gangrenous wall. Post-surgically, the gallstones were determined to be of cholesterol origin. What is cholelithiasis and cholecystitis?

A

Cholelithiasis= gallstones
Cholecystitis= inflammation of gallbladder

49
Q

Explain the reactions causing the production of reactive oxygen species in heart tissue.

A

The main sources of ROS in cardiac myocytes include NADPH oxidases, xanthine oxidase, nitric oxide synthase (NOS), and mitochondria

excessive cardiac ROS leads to abnormal electric function and indirectly decreases ATP generation

50
Q

How are reactive oxygen species neutralized in the heart tissue?

A

antioxidative enzymes (GPX and PRX-TRX) neutralize heart tissue

Theres a build up of NADH but the body is trying to get rid of it which leads to consequences
-try to make NADPH and NAD+ (NAD+ is a ROS)
-cant leave lots of NADH in system because it inhibits TCA, so it needs to be broken down and tried to be freed of this (but this ultimately leads to a heart attack if theres too much ROS)

SOD breaks down H2O2 into water, but if it cant keep up then it will accumulate and is bad because H2O2 is ROS

In normal instances, we used ROS to mainly produce nucleotide biosynthesis and alpha-KG

51
Q

Name the branches of the left coronary artery:

A

left circumflex artery, left marginal artery, left anterior descending artery (LAD)

52
Q

All of the following are treatments for MI EXCEPT:
A) inhibit pyruvate dehydrogenase
B) sodium glucose transport protein 2 (SGLT2) inhibitors
C) ACE inhibitor and angiotensin receptor blockers
D) malonyl CoA decarboxylase (MCD) inhibitors

A

A) inhibit pyruvate dehydrogenase

53
Q

What effects increasing heart rate?
A) decreased duration of diastole
B) decreased stroke volume
C) increased blood flow
D) all of the above

A

A) decreased duration of diastole

54
Q

What is the MOA of tpa?

A

converts plasminogen to plasmin

55
Q

What makes up a foam cell?

A

macrophages that have engulfed LDL

56
Q

What appears in the plasma soon after damage and indicates infarction, the most specific, and most sensitive of the serum markers:

A

troponin

Health Studies (14 decks)

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