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VF1 - Block 3 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Aortic stenosis is heard in systole or diastole?

A

systole

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2
Q

location of aortic stenosis murmur on physical exam

A
  • Upper right sternal border
  • Carotids
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3
Q

Shape of aortic stenosis murmur

A
  • Diamond-shaped in systole
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4
Q

Chest X-ray findings with aortic stenosis

A
  • Left Ventricular hypertrophy
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5
Q

Mitral regurgitation is heard in systole or diastole?

A
  • systole
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6
Q

Where do you hear mitral regurgitation on physical exam?

A
  • Cardiac apex
  • Axilla (armpit)
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7
Q

What is the shape of a mitral regurgitation murmur?

A
  • holosystolic
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8
Q

Pulmonic stenosis is heard in systole or diastole?

A

Systole

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9
Q

where can you hear pulmonic stenosis?

A
  • left upper sternal border
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10
Q

What is the shape of pulmonic stenosis murmur?

A
  • diamond-shaped
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11
Q

Chest X-ray findings for pulmonic stenosis?

A
  • Right ventricular hypertrophy
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12
Q

Chest X-ray findings for mitral stenosis?

A
  • Left atrial and left ventricular hypertrophy
  • Chronic: Also see right atrial and right ventricular hypertrophy
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13
Q

Tricuspid regurgitation is heard in systole or diastole?

A
  • Systole
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14
Q

Where do you hear tricuspid regurgitation on physical exam?

A
  • left lower sternal border radiating to right lower sternal border
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15
Q

Shape of tricuspid regurgitation murmur?

A
  • holosystolic
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16
Q

Chest X-ray findings of tricuspid regurgitation

A
  • Right atrial enlargement
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17
Q

Aortic regurgitation is heard in systiole or diastole?

A
  • diastole
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18
Q

aortic regurgitation is best heard where?

A

left sternal border

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19
Q

shape of aortic regurgitation murmur

A

de-crescendo

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20
Q

chest X-ray findings of aortic regurgitation

A
  • LV hypertrophy
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21
Q

mitral stenosis is heard in systole or diastole?

A

diastole

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22
Q

mitral stenosis is best heard where?

A

cardiac apex

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23
Q

shape of mitral stenosis murmur

A

low-pitched rumble, decresciendo-cresciendo associated with opening snap

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24
Q

Chest X-ray findings of mitral stenosis

A
  • left atrial enlargement
  • sometimes right ventricular enlargement
  • enlarged pulmonary arteries
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25
Q

pulmonic regurgitation is heard in systole or diastole?

A

diastole

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26
Q

pulmonic regurgitation is best heard where on physical exam?

A

left upper sternal border

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27
Q

shape of pulmonic regurgitation murmur

A

de-cresciendo

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28
Q

Chest X-ray findings of pulmonic regurgitation

A

RV hypertrophy

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29
Q

tricuspid stenosis is heard in systole or diastole?

A

diastole

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30
Q

location of tricuspid stenosis on physical exam

A

lower sternal border

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31
Q

shape of tricuspid stenosis murmur

A

low-pitched rumble, decresciendo-cresciendo, associated with opening snap

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32
Q

Chest X-ray findings of tricuspid stenosis

A

RA hypertrophy

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33
Q

Clonidine mechanism

A
  • activates alpha-2 receptors in the CNS
  • Binds presynaptic terminals to trick the CNS into thinking it does not need to release any more NE –> reduced sympathetic outflow
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34
Q

Clonidine use

A
  • Hypertension
  • ADHD
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35
Q

Clonidine side effects

A
  • CLONIDINE REBOUND
  • Hypotension
  • Dizziness and drowsiness
  • Dry mouth
  • Headache
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36
Q

alpha-methyldopa mechanism

A
  • Alpha-2 CNS agonist
  • Similar mechanism to clonidine
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37
Q

alpha-methyldopa uses

A
  • Hypertension in pregnant women
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38
Q

Sympathetic inhibitor side effects

A
  • Orthostatic hypotension
  • Head rush/syncope
    • Especially for alpha1 blockers
  • Activation of RAAS –> need diuretic to counteract these effects
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39
Q

Prazosin mechanism

A
  • Alpha-1 antagonist (vasculature)
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40
Q

Prazosin uses

A
  • Alpha-1 antagonist –> vasodilation
  • Used for hypertension
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41
Q

Prazosin side effect

A

First dose faint effect

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42
Q

hydralazine uses

A
  • hypertension
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43
Q

hydralazine mechanism

A
  • direct acting vasodilator
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44
Q

hydralazine side effects

A
  • rapidly lowers blood pressure
    • Results in reflex tachycardia
  • Headache
  • flushing
  • lupus-like symptoms
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45
Q

Why is cholesterol needed in normal cell function?

A
  • Membrane fluidity
  • Myelin sheath
  • Precursor for bile salts, vitamin D, steroid hormones
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46
Q

Where is cholesterol synthesized in the body?

A

Primarily hepatocytes (in the liver)

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47
Q

How is cholesterol regulated?

A
  • If cytosolic (intracellular) concentration is high, the cell will not make more cholesterol
  • The regulation depends on intracellular cytosolic cholesterol concentration
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48
Q

What is the first molecule in cholesterol synthesis?

A

Acetyl CoA

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49
Q

What is the rate limiting step in cholesterol synthesis?

A
  • HMG-CoA reductase
  • Inhibitors of HMG-CoA reductase inhibits cholesterol synthesis
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50
Q

What is the structure of a lipoprotein?

A
  • Phospholipid membrane
  • Triglycerides and cholesteryl esters in the hydrophobic core
  • Apoprotein can be within the core of lipoprotein OR the outside part. These apoproteins can act as receptors, enzyme inhibitors, enzyme activators, etc.
  • Cholesterol
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51
Q

How is cholesterol transported in the blood?

A

Lipoproteins

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52
Q

What are the main types of lipoproteins?

A
  • Chylomicrons
  • VLDL
  • LDL
  • HDL
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53
Q

What is the role of chylomicrons?

A
  • Transport dietary fat from intestines to the liver
  • Made by intestinal cells
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54
Q

What is the role of VLDL?

A
  • Transport large fatty acids from the liver to the systemic circulation
  • This type of cholesterol is atherogenic (promotes arterial plaques)
  • VLDL is converted to LDL, which is the worse type of cholesterol
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55
Q

What is the role of LDL?

A
  • Bad cholesterol
  • Transports lipids from liver to other organs where it is stored for later use
  • Highest percentage of cholesterol of all lipoproteins
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56
Q

what is the role of HDL?

A
  • Picks up cholesterol from peripheral cells and return them to the liver for excretion
  • This process is called reverse cholesterol transport
  • HDL is the good garbage man
  • High percentage of apolipoprotein
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57
Q

Overview of lipoprotein pathways

A
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58
Q

What is the job of lipoprotein pathways?

A
  1. When you eat, you want to distribute triglycerides to your cells – this is for energy.
  2. You want to supply cells with cholesterol b/c they need cholesterol for all sorts of things
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59
Q

There are more ______ (triglyceride or cholesterol esters) in chylomicrons?

A
  • Triglycerides
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60
Q

Characteristic apoprotein of chylomicron

A

B48

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61
Q

Role of lipoprotein lipase

A
  • Found on the wall of the capillaries
  • Takes triglyceride out of the lipoproteins
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62
Q

chylomicron remnant

A
  • Chylomicrons are formed in intestinal cells and then shipped to the liver through the blood
  • lipoprotein lipase removes triglycerides as chylomicrons move through the capillaries
  • Chylomicron remnants are what arrive at the liver
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63
Q

Describe the exogenous pathway

A
  • You eat and take dietary fat into the intestine
  • Intestinal cell synthesizes chylomicrons
    • More triglyceride than cholesterol ester in chylomicrons
    • B48 is the typical apoprotein of the chylomicron
  • Then chylomicrons go through capillaries, and the enzyme lipoprotein lipase is on capillary walls and hydrolyzes some free fatty acids from the chylomicron to supply FFA to adipose tissue and muscle.
  • When the chylomicrons come out of the capillaries, they’ve had triglycerides taken out and are referred to as a chylomicron remnant
  • This remnant gets taken up by the liver, broken down, and used for parts…
  • Liver releases bile acids and cholesterol back into the intestine. (That’s the end of the exogenous pathway.)
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64
Q

Describe the endogenous pathway

A
  • Liver makes VLDL from the things it has taken up from chylomicron remnants
    • VLDL is a precursor for LDL
      • It has more TG than cholesterol esters
      • It is characterized by B100 apoprotein
  • VLDL moves through the blood where lipoprotein lipase in capillaries strips out some of the triglycerides –> VLDL remnant, which is called IDL (intermediate density lipoprotein)
    • IDL has more cholesterol than triglycerides
    • Main apoprotein is apoprotein E​
  • IDL is converted to LDL in the blood (which is mostly cholesterol ester) OR taken up by the liver via endocytosis
  • LDL is taken up by liver via endocytosis OR sent to extrahepatic tissues
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65
Q

First step in endogenous lipoprotein pathway

A

Liver makes VLDL from chylomicron remnants

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66
Q

VLDL has more _____ (triglycerides or cholesterol esters)

A

triglycerides

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67
Q

apoprotein characteristic of VLDL

A

B100

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68
Q

what is IDL?

A
  • As VLDL moves through the blood, it gets triglycerides stripped out of it
  • IDL is the VLDL remnant
  • It gets converted to LDL in the blood OR returned to the liver
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69
Q

IDL has more _____ (triglycerides or cholesterol esters)

A

cholesterol esters

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70
Q

main apoprotein of IDL

A

apoprotein E

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71
Q

Where does LDL come from?

A
  • VLDL –> IDL –> LDL
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72
Q

Fate of LDL

A
  • Taken up by LDL receptors into the liver
  • OR sent to extrahepatic tissues and deposited
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73
Q

LDL receptor

A
  • Recognizes apoprotein B and apoprotein E
  • Takes up LDL
  • number of receptors are regulated by intracellular concentration of cholesterol
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74
Q

scavenger receptor type A

A
  • Recognize and endocytose damaged (oxidized) LDL
  • Found on macrophages
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75
Q

scavenger receptor type B

A
  • Mostly on liver
  • uptake HDL particles (or LDL)
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76
Q

What is the fuel transport pathway?

A
  • This is the pathway of distributing fatty acids to the cells after you eat
  • Starts in intestine when you eat
  • Fats/cholesterol packaged into chylomicrons
  • Chylomicrons deliver TG’s to cells for energy use
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77
Q

What is the overflow pathway?

A
  • Pathway of LDL metabolism
  • VLDL secreted by liver –> Overflow pathway –> LDL distributed to cells and then taken back to liver
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78
Q

As chylomicrons move through blood, what do they pick up?

A
  • More apoproteins from HDL
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79
Q

What happens to VLDL as it moves through blood?

A
  • Picks up more apoproteins from HDL
  • Interacts with LPL on endothelial cells and loses some of its triglycerides (some of these TG’s go to HDL, some go to muscle and fat)
  • Remnants of VLDL come back to liver and are converted to LDL on the surface of the liver, which then goes out and deposits cholesterol and cholesterol esters to the tissues via endocytosis.
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80
Q

Why is HDL considered good cholesterol?

A
  • It goes around to peripheral tissue and picks up cholesterol and other remnants
  • Returns to liver where HDL can be metabolized
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81
Q

ABCA1

A

•transfers cholesterol to HDL

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82
Q

Common Hypercholesterolemia

A

Most common form of dyslipidemia, polygenic, likely due to both genetic and environmental risk factors.

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83
Q

Familial Hypercholesterolemia (FH)

A
  • due to mutation in LDL receptor gene
  • LDL receptors normally mediate cellular uptake of remnant particles and LDL.
  • in FH the receptor is impaired or inhibited.
  • Very high cholesterol and LDL in plasma result.
  • Autosomal dominant inheritance.
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84
Q

Familial Defective Apolipoprotein B (FDB):

A

Due to mutation in ApoB100 that impairs its ability to bind to the LDL receptor, resulting in high plasma cholesterol.

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85
Q

Familial Combined Hyperlipidemia:

A
  • overproduction of ApoB100 –> increased production of VLDL and LDL.
  • Hypercholesterolemia level seen is variable and may occur alone or with hypertriglyceridemia.
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86
Q

Familial Dysbetalipoproteinemia:

A
  • Mutation in the ApoE gene
  • LDL does not bind ApoE as well
  • Accumulation of remnant particles and increased plasma cholesterol and triglycerides.
87
Q

LPL Deficiency:

A

Very rare, and results in extremely high levels of VLDL, chylomicrons, triglycerides in plasma.

88
Q

Abeta-lipoproteinemia:

A

Rare, due to a mutation in MTP (for Microsomal triglyceride Transfer Protein), which is involved in the cellular assembly of VLDL.

89
Q

Tangier Disease:

A
  • Loss of function mutations in ABCA1
  • ABCA1 normally helps cholesterol exit cells and and then be taken up by HDL as part of the reverse cholesterol transport pathway.
  • resulting in low plasma HDL
  • Named for Tangier Island, VA. where first families identified with the disease resided.
90
Q

LCAT Deficiency

A
  • LCAT is an enzyme responsible for removing cholesterol from blood/tissues and attaching it to lipoproteins
  • Deficiency results in low HDL
  • lipid accumulation leads to corneal clouding (‘fish eye disease’).
91
Q

CETP

A
  • Cholesterylester transfer protein
  • CETP is an enzyme responsible for moving cholesterol esters and triglycerides between VLDL, LDL, and HDL.
  • Lower CETP levels promote HDL formation.
  • Higher CETP –> lower HDL
92
Q

What are the drug classes for dyslipidemia/high cholesterol?

A
  • Statins: inhibit HMG-CoA reductase – starve cells of cholesterol
  • Ezetimibe: Inhibit cholesterol uptake via NPC1L1
  • Fibrates activate the transcription factor PPARα, which increases LPL expression and reduces VLDL production
93
Q

What is the cause and result of atherosclerosis?

A
  • Build up of cholesterol in the arterial wall.
  • Accumulation of macrophages induces chronic inflammation within the vessel wall.
  • Results in formation of atheromatous plaque.
  • Artery loses ability to constrict/dilate (no elasticity – aka “hardening”)
  • Rupture of plaque = MI and Stroke
94
Q

How do statins work?

A
  • Reduced synthesis of cholesterol by inhibiting HMG CoA Reductase
  • Increased clearance of LDL
    • When cholesterol synthesis is reduced, the cell responds by putting more LDL receptors on the surface. This further increases clearance of LDL from the blood.
95
Q

Statin side effects

A
  • Some drug-drug interactions (grapefruit juice b/c statins inhibit CYP3A4)
  • Rhabdomyolysis
    • This is extremely rare, but it’s basically the only significant side effect of statins. They are considered to be VERY safe.
96
Q

Ezetimibe mechanism of action?

A
  • Inhibits absorption of dietary cholesterol
  • Results in decreased production of chylomicrons –> decreased VLDL –> lowers LDL cholesterol
97
Q

When is ezetimibe used?

A

When statins alone are unable to lower LDL to acceptable levels, or if statin intolerant.

98
Q

Ezetimibe side effects

A

•Diarrhea, GI discomfort.

99
Q

What are fibrates? How do they work?

A
  • Cholesterol lowering drugs
  • Mechanism not completely understood
  • They think the drug interacts with PPAR-alpha
    • Normally PPAR-alpha gets activated by fatty acids. When PPAR-alpha is activated, it serves as a transcription factor that turns on genes involved in lipid metabolism. That’s a physiologic response that’s good.
    • We think fibrates are a PPAR-alpha agonist –> increased metabolism of lipids.
  • Drug: gemfibrozil –> increases HDL and reducing triglycerides
100
Q

gemfibrozil

A
  • Fibrate = cholesterol lowering drug
  • Mechanism: PPAR alpha agonist –> increased lipid metabolism. (But not completely understood)
  • Increases HDL, decreases triglycerides
101
Q

gemfibrozil side effects

A
  • myolysis (muscle soreness).
  • When combined with statins it increases the risk of rhabdomyolysis, but this is rare.
102
Q

What are nicotinic acid drugs? How do they work?

A
  • Treats dyslipidemia
  • Mechanism not completely understood
  • Results in a decrease in VLDL release from the liver –> decreased LDL and decreased TG’s
  • Side effects: FLUSHING (in almost all patients)
    • Hepatotoxicity
    • Myositis
    • Exacerbation of hyperglycemia, peptic ulcer disease, gout
  • These drugs aren’t used much anymore
103
Q

Niacin, Vitamin B3

A
  • Nicotinic acid drugs
  • Used to treat dyslipidemia
  • But not used that much anymore
104
Q

How do the PCSK9 inhibitors work?

A
  • Used to treat dyslipidemias
  • Monoclonal antibodies against PCSK9, a serine protease
  • These inhibit the enzyme that facilitates degradation of LDL surface receptor, which results in MORE LDL uptake into cells –> lowers blood cholesterol.
  • Only use these drugs in people who can’t use statins. They are VERY expensive.
105
Q

Does a larger or smaller ventricle experience more wall stress?

A
  • Larger
  • Law of LaPlace:
    • Wall Stress = (Pressure x radius)/ (2 x wall thickness)
  • Larger radius –> more wall stress
106
Q

How does increased preload affect PV curve?

A

Greater EDV –> greater stroke volume

107
Q

How does increased afterload affect PV curve?

A
  • Greater End Systolic Volume (can’t pump all the blood out)
  • Greater pressure generated
108
Q

How does increased contractility affect the PV curve?

A
  • Same EDV
  • Decreased end systolic volume (pump more blood out)
    • Results in increased stroke volume
109
Q

HFrEF occurs with systolic or diastolic dysfunction?

A

systolic

110
Q

Does a dilated heart suggest systolic or diastolic dysfunction?

A

systolic

111
Q

What does PV loop look like for systolic dysfunction?

A
  • Increased end systolic volume
    • can’t pump all the blood out
  • Increased end diastolic volume
    • b/c you already have leftover blood from the end of systole
112
Q

What are the short term responses to systolic dysfunction? Long term responses?

A
  • Low CO –>
  • RAAS activation
  • Sympathetic nervous system activation
  • ADH secretion

Long term: cell death due to increased myocardial work

113
Q

A hypertrophic heart suggests systolic or diastolic dysfunction?

A

diastolic

114
Q

HFpEF is associated with systolic or diastolic dysfunction?

A

diastolic

115
Q

What does diastolic dysfunction do to the PV loop?

A
  • Heart is thicker –> cannot expand as much to fill –> Reduced End diastolic volume
  • But also increased end diastolic pressure due to lower compliance of the heart
116
Q

What are the results of diastolic dysfunction in the short term? Long term?

A
  • Lower stroke volume –> lower CO –>
  • RAAS activation
  • SNS activation

Long term: ???? heart failure?

117
Q

What’s the most common cause of right ventricular dysfunction?

A

Left heart failure

118
Q

What are the most common causes of heart failure?

A
  • Hypertension
  • Coronary artery disease
119
Q

Common physical findings with left-sided heart failure

A
  • Pulmonary rales
  • PMI shifted laterally
  • Wheeze in lung (ronchi)
  • S3 gallop
  • Murmurs of mitral regurgitation
  • Pulsus alternans
120
Q

Common physical findings with right heart failure

A
  • Elevated JVP
  • Ascites
  • Murmur of tricuspid regurgitation
  • Hepatomegaly
  • Right ventricular heave
121
Q

Right heart failure vs. left heart failure symptoms

A

Left heart failure:

  • Dyspnea
  • Orthopnea
  • Nocturia

Right heart failure:

  • Fluid retension
  • Right upper quadrant discomfort
  • Decreased appetite, nausea
122
Q

Pulsus alternans

A
  • Only one beat every other time
  • Don’t understand why
  • A sign of advanced heart failure
123
Q

Elevated natiuretic peptide indicates…

A
  • Heart failure
  • Stretched myocytes secrete natiuretic peptide. The more stretched they are, the more of this peptide they secrete
124
Q

Lab tests you’d expect with heart failure

A
  • hyponatremia
  • hypokalemia
  • elevated natiuretic peptide
125
Q

Normal cardiac filling pressures

A

RA: 5

RV: 25/5

LA: 10

LV: 120/10

Aorta: 120/80

126
Q

What do cardiac pressures look like after an MI?

A
  • They are all elevated EXCEPT:
    • LV systolic pressure is lowered
    • Aortic systolic is lower
127
Q

NYHA classification

A

1 = asymptomatic

2 = somewhere between

3 = somewhere between

4 = symptoms at rest

128
Q

ischemic cardiomyopathy

A
  • Infarct –>
  • Systolic dysfunction –> remodeling –> dilated heart
129
Q

hypertensive cardiomyopathy

A
  • TPR high –> LV hypertrophy –> diastolic dysfunction
130
Q

Dilated cardiomyopathy

A
  • Biventricular enlargement + sometimes atrial enlargement
  • Distinguish from ischemic cardiomyopathy b/c ischemic usually just involves left ventricle
131
Q

Causes of dilated cardiomyopathy?

A
  • 30% idiopathic
  • Infections –> inflammation
  • Cocaine
  • hypothyroidism
132
Q

hypertrophic cardiomyopathy?

A
  • LV hypertrophy WITHOUT hypertension or aortic stenosis
  • Mostly genetic in origin
133
Q

Most common cause of sudden death in young people?

A
  • hypertrophic cardiomyopathy
  • Example is someone dropping dead after a marathon
134
Q

restrictive cardiomyopathy

A
  • Abnormally rigid ventricles but not necessarily thickened
  • VERY imparied diastolic dysfunction
  • Cause left AND right sided failure
135
Q

amyloidosis

A
  • a type of restrictive cardiomyopathy
  • Abnormal protein deposits in tissues, including heart
  • Leads to very stiff ventricles –> diastolic dysfunction
136
Q

What is the most common immediate cause of acute coronary syndrome?

A
  • plaque rupture –> thrombus –> coronary occlusion
137
Q

Mechanisms of coronary thrombosis?

A
  • Atherosclerosis –> plaque rupture AND dysfunctional epithelium
138
Q

Common causes of plaque rupture

A
  • Emotional stress (ie. driving in traffic)
  • Physical exertion (i.e. shoveling snow)
  • Inflammatory cytokines (ie. influenza)
  • Vulnerable plaque - by chance
139
Q

Outcomes of a coronary thrombus

A
  1. Clot is dissolved by your body’s own mechanisms
  2. Unstable angina - no serum biomarkers
  3. Non-ST-elevation MI - positive biomarkers
  4. STEMI - positive biomarkers
140
Q

Spectrum of acute coronary syndromes?

A

Unstable Angina

Non-ST elevation MI

STEMI

141
Q

Unstable angina, Non-ST elevation MI, STEMI – which show myocyte destruction?

A
  • Non-ST elevation MI
  • STEMI
  • **When there are positive biomarkers, there is myocardial damage**
142
Q

Magic time window for having no cell injury?

A

20 minutes

143
Q

What are the biomarkers to distinguish MI vs. angina?

A

cardiac troponins

144
Q

Symptoms of an MI

A
  • **Pressure in the chest
145
Q

Main treatments for STEMI

A
  • PCI (cath lab)
  • Fibrinolytic (clot buster)
146
Q

Medication management of acute coronary syndrome

A
  1. Aspirin + one other antiplatelet (Clopidogrel)
  2. Statin
  3. Anticoagulant in the first 24 hours (heparin)
  4. ACE inhibitor - to prevent remodeling
  5. Nitrates - reduce ischemia but not mortality
  6. Beta blocker
147
Q

Complications of an acute MI

A
  1. Stroke - thromboembolism
  2. Heart failure
  3. Ventricular septal defect
  4. pericarditis
148
Q

Most common cause of right ventricular MI?

A

Inferior wall blockage

149
Q

Physical sign of VSD?

A

Loud systolic murmur over the sternum

150
Q

Cause of pericarditis? Sign?

A
  • Inflammation of the pericardium
  • Untreated STEMI
  • Friction rub on exam
  • Fever, sharp pain with pleuritic tendency
151
Q

Is an acute valve lesion tolerated?

A

NO

152
Q

Causes of an acute valve lesion?

A
  • Acute aortic regurgitation
    • Endocartitis due to IV drug use
  • Acute mitral regurgitation
153
Q

Causes of chronic valve lesions?

A
  • High afterload
    • ex: aortic stenosis –> LV hypertrophy
  • Volume overload
    • ex: aortic regurgitation or mitral regurgitation
154
Q

Congenital causes of valvular disease?

A
  • Marfan’s syndrome –> Mitral regurgitation or aortic regurgitation
  • Bicuspid aortic valve
  • Mitral valve prolapse - i.e. born with a floppy valve
155
Q

Non-congenital causes of valvular disease?

A
  • endocarditis
  • Age-related stenosis
  • aortic dissection –> aortic regurgitation
  • papillary muscle infarction –> fucked up valves
  • Trauma
156
Q

primary vs. secondary valve dysfunction

A
  • primary = problem w/ valves themselves
  • secondary = problem w/ supporting structures (like papillary muscles)
157
Q

Symptoms of valvular disease?

A
  • heart failure symptoms
    • dyspnea
    • exercise intolerance/fatigue
    • fluid retention
  • arrhythmias
  • syncope/pre-syncope
  • angina
158
Q

Most common causes of aortic stenosis

A
  • Age –> calcifications
  • Bicuspid valve
  • Rheumatic disease (in developing world)
159
Q

Physical exam findings for aortic stenosis?

A
  • Systolic murmur
    • Diamond shaped
  • pulsus parvus et tardus (weak and delayed pulse contour)
  • S4 gallop maybe
  • Could be upstream effects
160
Q

Where might you hear aortic stenosis?

A
  • Right sternal border (as usual)
  • Carotids
  • Apex possible
161
Q

Indications for valve replacement in case of aortic stenosis?

A
  • SAD
    • syncope, angina, dyspnea
162
Q

TAVR

A

transcatheter aortic valve replacement

163
Q

Aortic stenosis pearls

A
  • Frequently associated with GI problems
  • Significant coronary artery disease is commonly co-occurring
164
Q

Most common causes of aortic regurgitation?

A
  • Aortic dissection
    • Marfan’s
  • Bicuspid valve
  • Calcific degeneration
  • Rheumatic
  • Endocarditis
165
Q

Is acute aortic regurgitation tolerated?

A

NO

166
Q

Physical exam findings for aortic regurgitation?

A
  • Diastolic murmur
    • decrescendo
  • 3rd or 4th left intercostal space (just left of sternal border)
  • Wide pulse pressure - high systolic and low diastolic
  • If acute: pulmonary rales
167
Q

Most common causes of mitral regurgitation

A
  • Mitral valve prolapse
  • Marfan’s
  • Endocarditis
  • Dilated or ischemic cardiomyopathy –> papillary muscles pull away from valve –> regurgitation
168
Q

Mitral regurgitation physical exam findings

A
  • Holosystolic murmur
  • At apex and sometimes at axilla (armpit)
  • Acute: rales
  • Pulmonary hypertension –> right heart failure
  • S3 gallop if LV is decompensated
169
Q

Mitral Regurgitation clinical pearls

A
  • Mitral regurgitation –> remodeling (LV dilation) –> more mitral regurgitation
  • Mitral valve prolapse is usually benign, but is the leading cause of need for mitral surgery
  • Once the LV has undergone significant deterioration, the benefit of surgery is far less clear
170
Q

Mitral regurgitation consequences

A
  • Atrial arrhythmias –> thromboembolism
  • LV remodeling (dilation) –> heart failure eventually
  • Upstream issues
171
Q

Treatment for mitral regurgitation

A
  • Acute: surgery
  • Chronic: decrease blood pressure, consider valve repair if LV ejection fraction is preserved
172
Q

How does chronic coronary artery disease present?

A

Angina

173
Q

EKG results of chronic CAD

A

ST-segment depression

174
Q

Provocation of angina

A
  • Exertion
  • Emotions
  • Cold air
  • Large meal
175
Q

Pathophysiology of chronic coronary artery disease?

A
  • Fixed vessel narrowing
  • Endothelial cell dysfunction
176
Q

Most common test given to grade chronic coronary artery disease?

A

Exercise stress test

177
Q

Treatment of chronic CAD

A
  • Prevent progression of atherosclerosis by treating
    • Hyperlipidemia
    • hypertension
    • diabetes
    • smoking
    • obesity
    • depression
    • substance abuse
178
Q

Medications for chronic CAD?

A
  • Beta blockers
    • reduce shear stress on heart
  • Aspirin, clopidogrel
  • STOP SMOKING
  • Nitrates to help with symptoms
  • Statins for lipids
179
Q

What is claudication?

A

Angina in the legs

180
Q

Symptoms of peripheral artery disease

A
  • Claudication
  • When really severe can have pain at rest
  • Foot ulcers due to lack of blood flow
181
Q

Diagnostic tests for peripheral artery disease

A
  • Ankle brachial index
    • Measures BP in upper extremities and lower extremities
  • Walking ABI
  • Ultrasound
    • blocked artery has a higher speed of blood flow through it
  • Angiogram
  • MRA
    • like an angiogram but with dye
  • CT angiography
182
Q

How is PAD treated?

A
  • Statins
  • Aspirin
  • Bypass
  • Angioplasty
  • EXERCISE improves claudication
183
Q

Abdominal aortic aneurysm is more common in males or females?

A

Males

It’s rare in females

184
Q

Major risk factors for abdominal aortic aneurysm

A

SMOKING

Age

Male

Family History

185
Q

Protective for abdominal aortic dissection

A

Female

Black

Diabetes

186
Q

Size at which abdominal aortic aneurysms need surgical repair

A

5.5 cm

187
Q

Who should be screened for abdominal aortic aneurysm

A
  • Men who have ever smoked
  • Anyone with a first degree relative of the problem
188
Q

Surgeries for abdominal aortic aneurysm

A
  1. Open repair - DeBakey (TEXAS)
  2. Stent grafting

**Stent grafting is much easier. Lower mortality rates in the first 30 days, but no difference at 2 years**

189
Q

Aortic dissection

A

Separation of the layers of the wall of the aorta

190
Q

Type A vs Type B aortic dissection

A

Type A = involves ascending aorta

Type B = does not involve ascending aorta

191
Q

Treatment for Type A vs. Type B aortic dissection

A
  • Type A = repair immediately
  • Type B = medical management is actual better outcomes than surgery
192
Q

Common presentation for an aortic dissection

A
  • Chest pain with RAPID onset
  • Usually described as a tearing pain
193
Q

What is cerebral vascular disease?

A
  • Atherosclerosis of the carotid arteries or cerebral vascular arteries
194
Q

Major concern with cerebral vascular disease

A

Stroke

195
Q

What surgeries are there for cerebral vascular disease?

A
  • Endarterectomy in the carotids
    • Go in and clean them out
    • Risk: more likely to have a heart attack afterwards
  • Angioplasty
    • Risk: more likely to have a stroke aftewards
196
Q

Medical management for cerebral vascular disease

A
  • Lower blood pressure
  • Statins
197
Q

Pericarditis hallmarks

A
  • Young healthy person
  • Sharp pain with breathing
  • Friction rub
  • Worse when lying down
198
Q

GERD hallmarks

A
  • acid-type of burning instead of heat (heat = angina)
  • relieved by antacids, not by nitroglycerin
  • Precipitated by eating and/or laying down
199
Q

Peptic ulcer disease hallmarks

A
  • Gnawing pain at night
  • After meals, not with exertion
  • Relieved by antacids, not nitro
200
Q

Esophageal spasm hallmarks

A
  • dysphagia (difficulty swallowing)
  • Weirdly can be relieved by nitro due to smooth muscle relaxation
201
Q

Biliary colic (gallbladder disease) hallmarks

A
  • Feels like they’re wearing a belt after a big meal
  • Precipitated by fatty foods
  • Not relieved by antacids or nitro
202
Q

Costochondritis hallmarks

A
  • Sternal pain worsened with palpation
  • Better when they take a deep breath
  • Relieved by anti-inflammatories or steroids
203
Q

Aortic Dissection hallmarks

A
  • Instantaneous onset of the worst thoracic pain of their entire life
  • SUDDEN SEVERE PAIN
204
Q

Aortic aneurysm hallmarks

A
  • Doesn’t typically cause any pain at all unless it’s pushing on something
  • “I have this throbbing right under my adam’s apple that i can feel”
205
Q

Pleurisy hallmarks

A
  • Wrose with a deep breath
  • Pleural rub on physical exam
206
Q

Pulmonary embolus hallmarks

A
  • Pleuritic pain
  • Shortness of breath
  • Hypoxia and tachycardia
  • History is very important:
    • Long flight
    • Surgery
    • Injury to the leg
    • Predisposition to clotting
207
Q

Atypical presentation of coronary disease in women

A
  • Positive stress test but NEGATIVE angiogram
  • Cause: abnormal microvasculature
208
Q

Heart Failure drugs that show mortality improvements vs. drugs that show only symptomatic benefits

A

Mortality improvements:

  • MRAs (spironolactone, eplerenone)
  • ACE inhibitors (or ARBs)
  • Beta blockers
  • Hydralazine/nitrate combination

Symptomatic benefits:

  • Digoxin
  • Loop and Thiazide diuretics
209
Q

What is the Dig effect?

A
  • Slurring of the T-wave on EKG
210
Q

Do not give Digoxin to these people

A

Renal problems

211
Q

First recommendation for people with chronic heart failure?

A

REDUCE SALT

212
Q

Lasix

A
  • Loop diuretic
  • “lasts” for “six” hours
  • Used to rapidly pull water off in a heart failure patient
213
Q

unique side effect of spironolactone

A

gynecomastia

214
Q

Do not give nitrates to these people..

A

Taking erectile dysfunction drugs

VF1 - Block 3 (7 decks)

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