Cardiovascular Flashcards

Question 1

Q

Danger Signals!
Acute Coronary Syndrome (ACS) Overview
1. Definition/Etiology
2. Clinical presentation
3. Lab/Diagnostics
4. Initial treatment

Answer

A

clinical presentations ranging from ST-elevation myocardial infarction (STEMI) to non-ST segment elevation MI (NSTEMI) and unstable angina
- may be provoked by physical exertion, emotional upset, or eating a heavy meal
Classic: middle-age to older man
- c/o onset of steady chest or substernal discomfort lasting >15 mins
- described as squeezing, tightness, crushing, a knot in center of chest
- heavy pressure; “an elephant sitting on my chest”
- or band-like
- may radiate to inner aspect of one or both arms, shoulders, neck, and/or jaw
- can radiate to back (interscapular region)

PE:
- may be diaphoretic
- have palpitations
- SOB
- N/A

Some women, elderly, and diabetics may have atypical presentations:
- epigastric discomfort
- indigestion
- N/A
- new-onset fatigue
- dizziness

Other times, pain is unpredictable or gets worse w/ rest (unstable angina)

Best diagnostic test: 12-lead EKG
- some pt w/ MI may have normal to nonspecific EKG
ALL pts w/ suspected ACS should be given aspirin dose of 162-325 mg to chew and swallow, unless contraindicated
CALL 911!!

Question 2

Q

Stable Angina: definition

Answer

A

Typical angina is usually brief: 2-5 mins
- relieved by rest and/or nitroglycerin
- precipitated by exercise, emotional upset, heavy meals, or lifting heavy objects

Question 3

Q

Unstable Angina: definition

Answer

A

occurs after minimal activity, or can occur at rest (rest angina)
- episodes become more frequent, severe, or prolonged
- does NOT respond to rest or nitroglycerin
- s/s can resemble a heart attack
- can severely limit physical activity
- if MI is present, unstable angina is considered a type of ACS

Question 4

Q

Heart Failure: Overview
1. Definition/Etiology
2. Clinical Presentation

Answer

A

Two types:
- heart failure w/ reduced EF (HFrEF) → EF <40% (systolic HF)
- heart failure w/ presevered EF → EF >50% (diastolic HF)

Multiple causes:
- CAD, arrhythmias cardiomyopathy, hypothyroidism, uncontrolled HTN
- uncompensation can be caused by ↑ Na intake and noncompliance w/ meds

- elderly pt reports SOB and lightheaded w/ minimal exertion
  - can progress to dyspnea at rest
  - easily fatigued w/ even light exertion
  - orthopnea; sudden awakening from sleep (recumbent position) d/t severe SOB → relieved w/ upright/sitting position (paroxysmal nocturnal dyspnea)
  - peripheral edema caused by fluid retention
  - can be accompanied by poor appetite and RUQ abdominal pain

PE:
- lung crackles
- wheezing
- tachypnea
- tachycardia
- S3 gallop
- paradoxical splitting of S2
- JVD
- peripheral edema
- hypoxia

Question 5

Q

Infective Endocarditis
1. Definition/Etiology
2. Clinical Presentation
3. Lab/Diagnostics

Answer

A

AKA bacterial endocarditis
RF:
- valvular abnormalities
- arrhythmias
- IV drug use
- hemodialysis

Most common pathogens: MSSA and MRSA

- fever (up to 90.0ºF)
  - chills
  - new onset murmur (up to 85%)
  - anorexa
  - weight loss
  - associated skin findings are mostly on fingers/hands and toes/feet
  ► subungual hemorrhages (splinter hemorrhages on nailbed)
  ► petechiae on palate
  ► painful violet-colored nodes on fingers/toes (Osler nodes)
  ► nontender red stops on palms/soles (Janeway lesions)
  - funduscopic exam → may show Roth spots (retinal hemorrhages)
Initial: Transthoracic echocardiogram (TTE)

Question 6

Q

Abdominal Aortic Aneurysm
1. Definition/Etiology
2. Clinical Presentation
3. Initial lab/diagnostics

Answer

A

Highest risk factor characteristics: 70-yea-rold elderly white male, smoker (current or has quit), and has HTN (usually uncontrolled)
- most are asymptomatic
  - If NOT ruptured but has sx → abdominal, back, or flank pain

Classic s/s:
- severe, sharp, excruciating pain in abdomen, flank, and/or back
- w’ pulsatile abdominal mass (~50% cases)

Initial exam: Ultrasound
CXR: incidental findings of: widen mediastinum, tracheal deviation, and obliteration of aortic knob (thoracic aortic dissection)

Question 7

Q

Normal Findings: Anatomy → Position of the Heart
- Where is the apical impulse?

Answer

A

Right ventricle is chamber of heart that lies closest to the sternum
- The lower border of the left ventricle is where the apical impulse is generated
- heart is roughly the size of a large adult first
- apex beat is caused by the left ventricle

Apical impulse: located at the 5th intercostal space (ICS) by the midclavicular line on the left side of the chest

Question 8

Q

Displacement of the Point of Maximal Impulse (PMI): Causes

Answer

A

Severe L ventricular hypertrophy (LVH) and cardiomyopathy
- PMI is displaced laterally on chest and is >3 cm larger in size and more prominent
Pregnancy, third trimester
- as uterus grows, it pushes against diaphragm and causes heart to shift to left of the chest anteriorly → displaced PMI, located slightly upward on left side of chest
- May hear S3 during pregnancy

Question 9

Q

Deoxygenated Blood pathway and physiology

Answer

A

enters heart through superior vena cava and inferior vena cava

Right Atrium → Tricuspid valve → Right ventricle → pulmonic valve → pulmonary artery → the lungs → alveoli (RBBCs pick up oxygen and release carbon dioxide)

Question 10

Q

Oxygenated blood pathway and physiology

Answer

A

Exits the lungs through the pulmonary veins and enters the heart

Left atrium → mitral valve → left ventricle → aortic valve → arch → general circulation

Question 11

Q

Systole and Diastole valves

Answer

A

“Motivated Apples” → reminds you of names of valves) which produces sound, and type of valve (atrioventricular [AV] or semilunar valves)

Motivated:
M: mitral
T: tricuspid
AV: atrioventricular (AV) valves

Apples
A: aortic
P: pulmonic
S: semilunar valves

Question 12

Q

Heart Sounds:
1. S1
2. S2
3. S3
4. S4

Answer

A

Systole; “Motivated” → M = mitral, T = tricuspid, AV = AV valves
- the “lub” sound (of “lub dub”)
- Closure of the mitral and tricuspid valves
- AV valves
Diastole; “Apples” → A = aortic, P = pulmonic, Semilunar valves
- the “dub” sound (of “lub dub”)
- Closure of the aortic and pulmonic valves
- Semilunar valves
- usually indicates HF or CHF
  - occurs during early diastole (also called a “ventricular gallop” or an “S3 gallop”)
  - Sounds like “Kentucky”
  - ALWAYS considered abnormal if it occurs after >40 years
  - Can be normal finding in children, pregnant women, and some athletes (>35 years)
- ↑ resistance d/t stiff LV; usually indicates LVH
  - Considered a normal finding in some elderly (slight stiffness of LV)
  - Occurs during late diastole (also called an “atrial gallop” or “atrial kick”)
  - Sounds like “Tennessee”
  - Best heard at the apex (for apical area; mitral area) using bell of stethoscope

Question 13

Q

Stethoscope Skills:
1. Bell of stethoscope
2. Diaphragm of stethoscope

Answer

A

- low tones such as extra heart sounds (S3, S4)
  - Mitral stenosis
- mid- to high-pitched tones (such as LS)
  - mitral regurgitation
  - aortic stenosis

Question 14

Q

Heart Sounds: Benign variants
1. Physiological S2 split
2. S4 in the elderly

Answer

A

Best heard over pulmonic area (or 2nc ICS on the upper left side of sternum)
- caused by splitting of aortic and pulmonic components
- a normal finding if appears during inspiration and disappears at expiration
- Some healthy elderly pts have S4 (late diastole) heart sound
  - AKA “atrial kick” ; the atria has to squeeze harder to overcome resistance of a stiff LV
  - if no s/s of heart/valvular ds → normal variant
  - Pathological S4 is associated w/ LVH d/t ↑ resistance from LV

Question 15

Q

Solving Questions: Heart Murmurs Instructions

Answer

A

Look for timing of murmur (systole or diastole?)
Look for location of murmur
- aortic
- Erb’s point
- mitral area

All murmurs seen on exam will fit into two mnemonics:

Timing:
Systolic Murmurs: MR. ASS
Diastolic Murmurs: MS. ARD

Question 16

Q

Murmurs: MR. ASS

Answer

A

Systolic Murmurs:
- occurring during S1
- AKA holosystolic, pansystolic, early systolic, late systolic or midsystolic murmurs
- compared w/ diastolic murmurs, these are louder and can radiate to neck or axillae

Mitral Regurgitation
- pansystolic (or holosystolic) murmur
- best heard at apex (or apical area) of heart
- may radiate to axilla
- loud blowing and high-pitched murmur (use diaphragm of stethoscope)

Aortic Stenosis
- midsystolic ejection murmur
- best heard at 2nd ICS at R side of sternum
- may radiate to nec
- harsh and noisy murmur (use diaphragm of stethoscope
** Pts w/ AS should avoid physical overexertion → ↑ risk of sudden death → Refer to cardiologist
- Monitored by serial cardiac sonograms w/ Doppler flow studies; surgical valve replacement needed if worsens

Question 17

Q

Murmurs: MS. ARD

Answer

A

Diastolic Murmurs:
- AKA S2 heart sound, early diastole, late diastole, or mid-diastole
- ALWYAS indicative of heart ds (unlike systolic murmurs)

Mitral Stenosis
- a low-pitched diastolic rumbling murmur
- best heard at apex (or apical area) of heart
- AKA opening snap (use bell of stethoscope)

Aortic Regurgitation
- A high-pitched diastolic murmur (use diaphragm of stethoscope)
- If AR is d/t diseased aortic valve, murmur is located at 3rd ICS by L
sternal border (Erb’s point)
- If AR is d/t abnormal aortic root, murmur is best heard at R upper sternal border (aortic area)

Question 18

Q

Auscultatory Areas: Location

Answer

A

Mitral area
- apex (or apical) area of the heart
- 5th L ICS approximately 8-9 cm from midsternal line, slightly medial to midclavicular line
- PMI or apical pulse is located here

Aortic area
- 2nd ICS to right side of the upper border of sternum
- AKA “2nd ICS by right side of sternum at base of heart”
- also be described as a murmur that is located on R side of the upper sternum

Erb’s point
- 3-4th ICS on left sternal border

Question 19

Q

Heart Murmurs: Grading System

Answer

A

Grade: Description
I → A very soft murmur heard only under optimal conditions

II → A mild to moderately loud murmur

III → Loud murmur, easily heard once stethoscope is placed on chest

IV → Louder murmur; first time that a thrill is present; a thrill is like a “palpable murmur”

V → Very loud murmur, heard w/ edge of stethoscope off chest; thrill is more obvious

VI → Murmur so loud, can be heard even w/ stethoscope off chest; thrill is easily palpated

Question 20

Q

Abnormal Findings: Pathological Murmurs Overview

Answer

A

All diastolic murmurs are abnormal
All benign murmurs occur during systole (S2)
Benign murmurs do NOT have a thrill; only very loud murmurs will produce a thrill

Question 21

Q

Atrial Fibrillation and Atrial Flutter
1. Definition/Etiology
2. Risk Factors
3. Clinical Presentation

Answer

A

AFib → most common cardiac arrhythmia in US
- major cause of stroke
- classified as supraventricular tachyarrhythmia

Aflutter → atrial beat regularly but faster than usual (e.g., 4 atrial beats per one ventricular beat)

Both have similar treatments
Risk of stroke/death is higher in elderly pts

Paroxysmal AF (intermittent or self-terminating): episodes terminate within 7 days or less (usually <24 hrs); usually asymptomatic

- HTN, CAD, ACS, stimulants caffeine, cocaine, nicotine, amphetamine), hyperthyroidism, alcohol intake (“holiday heart”), heart failure, LVH, pulmonary embolism (PE), COPD, sleep apnea, etc
- sudden onset of heart palpitations, described as “a fish is flopping in my chest” or “drums are pounding in my chest”
  - accompanied by feelings of weakness, dizziness, and tachycardia
  - reduction of exercise capacity
  - may c/o dyspnea, chest pain, and feeling like passing out (presyncope to syncope)
  - rapid and irregular pulse
  - may be >100 bpm w/ mild hypotension
  - AF can be paroxysmal and can stop spontaneously (w/in 7 days) or can be long-standing and persistent (>12 ms)

** if hemodynamically unstable (chest pain/angina, hypotension, HF, cold clammy skin, AKI) w/ new onset of AF w/ severe symptoms → Call 911!

Question 22

Q

Afib/flutter
4. Lab/Diagnostics

Answer

A

Search for underlying cause!
Every pt w/ AF needs to be evaluated for anticoagulation therapy
→ CHA2DS2-VASc score: helps determine if pt needs anticoagulation therapy

C → CHF
H → HTN
A → Age 65-74 years
D → Diabetes
S → Sex; F gender is at higher risk

Score:
0 = low risk
≥2 = requires anticoagulation; some physicians will tx pt w/ score of 1

Diagnostic test: 12-lead EKG
- does not show discrete P waves
- irregularly irregular rhythm (Afib)

New onset labs:
- EKG
- thyroid-stimulating hormone (TSH)
- electrolytes (Ca, K, Mg, Na)
- renal function
- BNP (r/o HF)
- troponin (r/o MI)
- consider 24-hr Holter monitor is paroxysmal AF
- Digoxin level (if on digoxin)
- ECHO (r/o valvular pathology, ↑ risks of stroke)
- Lifestyle: avoid stimulants (caffeine, nicotine, decongestants, alcohol)

Question 23

Q

Afib/flutter Medications

Answer

A

Referred to cardiologist for medical management
+ Option w/ new-onset AF w/ stable pts is cardioversion (first 48 hrs) or rate control

Management varies on bases of AF severity and symptoms

Rate Control:
- Betablockers, CCBs, digoxin
- Amiodarone (Cordarone; antiarrhythmic) → BBW of pulmonary toxicity, hepatic injury, hyper- or hypothyroidism, visual impairment, peripheral neuropathy, and worsened arrhythmia

Anticoagulation
- Warfarin (Coumadin; vit K antagonist) → for pts w/ abnormal or damaged heart valves and ES-CKD; needs baseline INR, aPTT, CBC (check platelets), creatinine, and LFTs
- Initial daily dose ≤5 mg, but frail, sensitive, or elderly pts >79 should take lower dose (2.5 mg)
- Full anticoagulation effect can take 3 days; check INR Q2-3 days until therapeutic for 2 consecutive checks; then recheck weekly, so on until INR is stable at 2-3
- check Q4wks when stable
* Refer to institutional protocols or refer to anticoagulation clinic; refer to cardiologist if lack experience
* FDA category X drug; teratogenic!

► Warfarn goal for Afib: INR 2.0-3.0
► synthetic/prosthetic valves: INR 2.5-3.5

If bleeding episode suspect → INR check with PT and PTT
* Warfarin drug interactions (see notecard)

Direct-acting anticoagulants (DOACs): FIRST line agents for nonvalvular AF
Ex: dabigatran (Pradaxa), rivaroxaban (Xarelto), edoxaban (Savaysa), apixaban (Eliquis)
→ Advise pt to take meds on schedule and do NOT skip doses (effect is lost after 12 hrs); do NOT require INR monitoring, have no major dietary restrictions, have have fewer drug interactions

Platelet inhibitors (clopidogrel [Plavix]) either alone or in combo w/ aspirin and other anticoagulants; may be better tolerated but less effective than DOACs and warfarin

Alcohol abstinence ↓ risk of recurrent AF even among regular drinkers

Question 24

Q

Afib/flutter: Warfarin drug interactions that can ↑ INR

Answer

A

Glucocorticoids (Methylprednisolone, prednisone)
SSRIs and SNRIs (Fluoxetine, sertraline, duloxetine, fluvoxamine, venlafaxine)
Fluoroquinolones (Ciprofloxacin, levofloxacin, moxifloxacin, norfloxacin)
Macrolides (Azithromycin, clarithromycin, erythromycin)
Penicillins (amoxicillin, amoxicillin-clavulanate)
Azole antifungals (fluconazole, miconazole)
Statins (fluvastatin, lovastatin, rosuvastatin, simvastatin)
Others: Tramadol, fenofibrate, trimethopri-sulfamethoxazole

Question 25

Q

Afib/flutter Complications

Answer

A

Death caused by thromboembolic even (e.g., stroke, PE), CHF, angina, and others
Warfarin-associated intracerebral hemorrhage has high mortality and causes 90% of warfarin deaths; medical emergency, call 911!
Warfarin-associated life-threatening bleeding episode: stop warfarin and ALL anticoagulants such as acetylsalicylic acid (ASA) and NSAIDs; treat w/ vit k, 4-factor prothrombin complex concentrate (PCC, inactivated), and/or fresh frozen plasma
► check INR, PT, and PTT
DOAC-associated life-threatening bleeding episode: life-threatening bleeding caused by rivaroxaban (Xarelto) and apixaban (Eliquis); can be tx w/ andaxanet alfa (Anexxa)
bleeding caused by dabigatran (Pradaxa) is tx w/ idarucizumab (Praxbind)

Question 26

Q

Patient Education: Dietary Sources of Vitamin K

Answer

A

Warfarin only, does NOT apply to Direct-Acting Anticoagulants

Advise pts to be consistent w/ their day-to-day consumption of vit K foods
Give pt a list of foods w/ high levels of vit K (“greens” such as kale, collard, mustard, spinach, iceberg or romaine lettuce, brussels sprouts, potatoes)
Only one serving/day is recommended for very high vit K foods

Question 27

Q

Elevated INR: What should you do?
1. if INR <4.5?
2. if INR 4.5-10

Answer

A

Presence of bleeding: None
► Skip next dose and/or reduce slightly the maintenance dose; check INR once or twice a week when adjusting dose
- do NOT give vit K
- if INR elevation is minimal, often maintenance dose does not need to be ↓
Presence of bleeding: None or not clinically significant bleeding
► Hold 1-2 doses; with or without administration of low-dose oral vit K (1-2.5 mg)
- Monitor INR Q2-3 days until stable
- ↓ warfarin maintenance dose

Question 28

Q

Paroxysmal Supraventricular Tachycardia (PSVT)
1. Definition/Etiology
2. Clinical presentation
3. Lab/Diagnostics
4. Treatment

Answer

A

tachycardia w/ peaked QRS complex w/ P waves present
- regular but rapid heartbeat, which starts and stops abruptly (intermittent episodes)
- can be misdiagnosed as panic or anxiety attack
- PSVT → part of the narrow QRS complex tachycardias w/ regular ventricular response (several types including Wolff-Parkinson-White [WPW] syndrome, atrial tachycardia)
- can start in childhood or older
- may resolve spontaneously or reoccur at a later time

Episodes can be precipitated by digitalis toxicity, alcohol, hyperthyroidism, caffeine intake, and illegal drug use

- abrupt onset of palpitations (“feels like fluttering in my chest”)
  - rapid pulse (150-250 bpm)
  - lightheadedness
  - SOB
  - anxiety
  - may feel weak and fatigue or faint
  - may report previous episode that resolved spontaneously
- EKG; if WPW or symptomatic → Refer to cardiologist
- if hemodynamically unstable → may require cardioversion → call 911!
  - Vagal maneuvers for acute treatment of SVT; several types

Question 29

Q

Wolff-Parkinson-White (WPW) syndrome

Answer

A

narrow QRS complex tachycardia → ↑ risk for death
→ Refer to cardiology for catheter ablation

Question 30

Q

SVT Vagal maneuvers

Answer

A

Vagal maneuvers:
- carotid massage → pt supine, monitor VS
* If done in clinical setting, continuous 12-lead EKG during procedure
- responses are changes in HR or rhythm and/or BP after sinus massage

Sinus massage contraindications:
- TIA or stroke within previous 3 months
- presence of carotid bruits and so forth

Valsalva’s maneuver
- Holding one’s breath and straining hard
- maintain strain for 10-15 seconds, release, then breath normally

Question 31

Q

Pulsus Paradoxus
1. Definition/Etiology
2. Pulmonary Causes
3. Cardiac Causes

Answer

A

fall in SBP of >10 mm Hg during inspiraotry phase
- AKA paradoxical pulse
- important physical sign of cardiac tamponade
- certain pulmonary and cardiac conditions that impair diastolic filling can cause an exaggerated ↓ of intrathoracic pressure during inspiration
- asthma
  - emphysema (↑ positive pressure)
- cardiac tamponade
  - pericarditis
  - cardiac effusion (↓ movement of LV)

Question 32

Q

EKG Interpretation

Answer

A

Know “irregularly irregular rhythm w/ no visible p-waves” → Afib

Memorize:
- Afib
- anterior wall MI (ST segment elevations in lead V2-V4)
- Ventricular tachycardia (jagged irregular QRS)
- SR, sinus arrhythmia

PR interval (atrial depolarization): 0.12-0.2 seconds (3-5 small boxes)

Question 33

Q

Anterior Wall Myocardial infarction

Answer

A

AKA anterior STEMI
most common type of MI

EKG changes include:
- ST segment elevation and Q waves
- Wide QRS complex in leads V2 to V4
- resembles a “tombstone” → “tombstoning”

Question 34

Q

Sinus Rhythm and Sinus Arrhythmia

Answer

A

Sinus Arrhythmia → common variation of NSR
- more common in healthy children and young adults
- P waves show uniform morphology
- PP interval increases and decreases during inspiration and exhalation

Question 35

Q

Hypertension
1. Definition/Types
- ACA/AHA HTN guidelines
2. Initial treatment considerations

Answer

A

HTN = BP >130/80 mmHg

majority: Primary/essential HTN
~5-10% have secondary HTN

- Nonpharmacologic tx/lifestyle changes recommended for majority of adults who are newly classified
  - If presence of RF (e..g, diabetes, CAD, HTN), pharmacologic therapy is recommended w/ lifestyle

► ANCC uses 2017 ACC/AHA
► AANPCB uses both 2017 ACA/AHA HTN guidelines and JNC 8 guidelines

Question 36

Q

Hypertension: Correct BP Measurement

Answer

A

Instruct pt to avoid smoking or caffeine intake 30 mins before measurement and not cross their legs (↑ SBP)
Begin BP measurement after at least 5 mins of rest (mercury sphygmomanometer preferred over digital machines)
≥2 reading separated by 2 mins should be averaged per visit
High # determines BP stage (BP 140/100 is stage 2 instead of stage 1)

Question 37

Q

HTN: BP stages
1. Normal
2. Elevated
3. Stage 1
4. Stage 2

Answer

A

SBP <120 and DBP <80
SBP 120-129 and DBP <80
SBP 130-139 or DBP 80-89
SBP >140 or >90

Question 38

Q

HTN screening

Answer

A

Start at 18 years
screen BP every year
If normal, recheck in 1 year
If presence of RF for HTN, screen at least semiannually (twice a year)

Question 39

Q

Relationship between Blood Pressure, Peripheral Vascular Resistance, and Cardiac Output

Answer

A

Any changes in peripheral vascular resistance (PVR) or cardiac output (CO) → change in BP (increase/decrease)

EX:
Na (sodium)
- Water retention ↑ vascular volume → ↑ CO, BP ↑
- Younger pts and whites have ↑ renin levels compared w/ the elderly

Angiotensin I to Angiotensin II: Angiotensin II ↑ vasoconstriction and will ↑ PVR → ↑ BP

Sympathetic System Stimulation: Epinephrine and cortisol secretion → tachycardia and vasoconstriction → ↑ BP

Alpha-blockers, Beta-blockers, CCB: Drugs ↓ PVR from vasodilation → ↓ BP

Pregnancy
- SVR is ↓ d/t hormones (SBP and DBP ↓ during 1st and 2nd trimesters)
- S3 heart sounds is common in 3rd trimester of pregnancy
- Drugs used to control BP in pregnancy are methyldopa, labetalol, beta-blockers, and diuretics

Question 40

Q

HTN: Labs (by systems)

Answer

A

Kidneys
- Creatinine
- eGFR
- urinalysis

Endocrine
- TSH
- fasting BG

Electrolytes: K, Na, Ca

Heart
- cholesterol
- HDL
- LDL
- triglycerides
- complete lipid panel

Anemia: CBC

Baseline EKG and CXR (to r/o cardiomegaly)

Question 41

Q

HTN: Rule out Target Organ Damage - Microvascular Damage

Answer

A

Eyes (hypertensive retinopathy)
- Silver and/or copper wire arterioles
- arteriovenous junction nicking (caused when arteriole crosses on top of a vein)
- Flame-shaped hemorrhages
- papilledema

Kidneys
- microalbuminuria and proteinuria
- ↑ serum creatinine and abnormal eGFR (r/o kidney ds)
- Peripheral and generalized edema

Question 42

Q

HTN: Hypertensive retinopathy features

Answer

A

Silver and/or copper wire arterioles
arteriovenous junction nicking (caused when arteriole crosses on top of a vein)
Flame-shaped hemorrhages
papilledema

Question 43

Q

HTN: Possible kidney ds features

Answer

A

microalbuminuria and proteinuria
↑ serum creatinine and abnormal eGFR (r/o kidney ds)
Peripheral and generalized edema

Question 44

Q

HTN: Rule out Target Organ Damage - Macrovascular Damage

Answer

A

Heart
- S3 (CHF)
- S4 (LVH)
- Carotid bruits (narrowing d/t plaque, ↑ risk of CAD)
- CAD and acute MI
- ↓ or absent peripheral pulses (PAD)

Brain
- TIAs
- Hemorrhagic strokes

Question 45

Q

Secondary HTN
1. Definition
2. 3 Major Groups (organ systems)

Answer

A

HTN caused by another condition; if condition is corrected and/or treatable, then HTN will resolve
- 5-10% are secondary HTN
** R/o secondary cause and maintain a high index of suspicion if the following:
- <30 years
- Severe HTN or acute rise in BP (previously stable pt)
- Resistant HTN despite tx w/ at least 3 antihypertensive agents
- Malignant HTN
► Renal
- renal artery stenosis
* more common in younger adults
- polycystic kidneys
- CKD
* more common in elderly pts

► Endocrine
* middle-age adults more likely to have endocrine-related ds
- hyperthyroidism
- hyperaldosteronism
- pheochromocytoma

► Others
- OSA
* sleep partner will report severe snowing w/ apneic episodes during sleep
- marked hypoxic episodes during sleep ↑ BP
- coarctation of the aorta (see notecard)

Question 46

Q

What is Malignant HTN?

Answer

A

severe HTN w/ end-organ damage such as retinal hemorrhages, papilledema, acute renal failure, and severe headache

Question 47

Q

Secondary HTN: Coarctation of the aorta

Answer

A

Normal: SBP is higher in legs (normal finding) because it takes more force to circulate blood back tp the heart

In coarctation, opposite is true. If there is a narrowed aorta in abdomen (abdominal aorta), the part of the bode above the narrowed aorta (arms) will have higher BP and bounding pulses. The part of the body below the narrowed aorta (legs) will have lesser blood flow, so SBP on legs will be lower, and pulses will be weaker.

Look for delayed or diminished femoral pulses
Check both radial and femoral pulse at the same time and compare

Question 48

Q

Clinical findings of Secondary HTN: Kidneys

Answer

A

Bruit epigastric, abdomen, or flank area → Renal artery stenosis

Tx: avoid ACEi and ARBs

Enlarged kidneys w/ cystic renal masses (polycystic kidneys)

-↑ creatinine and ↓ eGFR (renal insufficiency to AKI)

Question 49

Q

Clinical findings of Secondary HTN: Endocrine - Conn’s syndrome

Answer

A

Primary hyperaldosteronism (Conn’s syndrome):
* Aldosterone helps control BP by Na retention and loss of K
* most common cause is an aldosterone-producing adenoma (usually benign); less commonly, adrenal CA

S/s
- HTN w/ hypokalemia (low K) is usually the only sign of this condition
- Normal to elevated Na levels (high/normal Na+)

Tx: surgical removal of tumor

Question 50

Q

Clinical findings of Secondary HTN: Endocrine - Hyperthyroidism

Answer

A

S/S + diagnostics
- weight loss
- tachycardia
- fine tremor
- moist skin
- anxiety
- new onset of AF (check EKG)
- Check TSH

Question 51

Q

Clinical findings of Secondary HTN: Endocrine - Pheochromocytoma

Answer

A

excessive secretion of catecholamines → severe HTN, arrhythmias
Labile ↑ in BP accompanied by palpitations
Sudden onset of anxiety, sweating, severe headache
Order plasma-free metanephrine (high-risk pt) or urine metanephrines fractionated (low risk pt)

Question 52

Q

How to diagnose HTN

Answer

A

Check BP (serial BP)
Confirm diagnosis at another subsequent visit 1-4 wks after initial visit
Check BP at home and keep diary
Does office BP correlate w/ home BP?
Advise pt to bring their BP monitor to office so it can be checked against the office’s machine
Difference of ≤ 5 mmHg, not significant
if home NP are lower, rule out “white coat” HTN → to r/o, have pt check their BP outside of clinic several times and compare w/ office BP → if home readings do not meet criteria for HTN, it is white coat HTN

Question 53

Q

HTN: Self-measured BP

Answer

A

useful adjunct to supplement office readings
Advise pt to buy an automatic BP machine
Advise obese pt to buy a model w/ the larger-sized BP cuff (pt should measure diameter of upper arm)
if cuff is too small → false elevate BP
Advise pt to check BP at different times of day and during work
Instruct pt to bring their BP diary during visits if titrating meds
BP kiosk readings are acceptable

Question 54

Q

Hypertensive Urgency

Answer

A

SBP >180 and/or DBP >120
WITHOUT target organ damage

Common reason: noncompliance w/ antihypertensive therapy
- if no clinical (or lab) evidence of new or worsening target organ damage, restart or intensify antihypertensive drug therapy w/ close follow-up

Question 55

Q

Hypertensive Emergency

Answer

A

SBP >180 and/or DBP >120 WITH clinical findings of target organ damage

such as…
- N/V
- ↑ ICP
- CVA/TIA
- MI
- acute PE
- ARF
- retinopathy (flame-shaped hemorrhages)
- papilledema
- acute severe low-back pain (dissecting aorta)

CALL 911!

Question 56

Q

Marked Hypertension

Answer

A

Defined as SBP 120-129 w/ normal DBP <80 after 3-month lifestyle modification trial, while daytime home measurement BP is 130/80 or higher

Question 57

Q

Isolated Systolic HTN in the Elderly

Answer

A

caused by loss of recoil in arteries (atherosclerosis) → ↑ PVR
Pulse pressure ↑
emphasize nonpharmacologic tx, esp dietary salt restriction and weight loss in obese
Treat BP in older or frailer pts carefully (high fall risk, orthostatic hypotension); start at lower doses and titrate up slowly; will take 3-6 months

Initial monotherapy w/ a low-dose thiazide diuretic, a CCB (long-acting dehydropyridine) or an ACEi or ARB

Question 58

Q

Pulse pressure

Answer

A

SBP - DBP

Question 59

Q

Orthostatic Hypotension

Answer

A

Elderly at higher risk d/t less active autonomic NS and slower metabolism of drugs by liver (prolongs half-life of drugs)

To evaluate for orthostatic hypotension:
- check BP in both supine and standing positions, esp in elderly, before and after treatment for HTN
- check for polypharmacy → carefully review med hx and search for meds that ↓ BP
- Ask pt if dizzy or lightheaded w/ changes in position

Question 60

Q

Guideline for the Prevention, Detection, Evaluation, and Management of High BP in Adults: Assessment Considerations

Answer

A

First, assess 10-year risk for heart ds using ASCVD
Reassess in 1 month for effectiveness of BP-lowering med therapy
If goal is met in 1 month, reassess in 3-6 months
If goal is NOT met in 1 month, consider different med or titration
Continue monthly follow-up until BP control is achieved

Normal: SBP <120, DBP <80

Encourage heart-healthy lifestyle, evaluate yearly

Question 61

Q

Guideline for the Prevention, Detection, Evaluation, and Management of High BP in Adults: Elevated BP

Answer

A

SBP 120-129, DBP <80

Recommend heart-health lifestyle and weight loss if overweight/obese

Reassess in 306 months
No more “prehypertension” stage; instead, it is known as “elevated BP”

Question 62

Q

Guideline for the Prevention, Detection, Evaluation, and Management of High BP in Adults: HTN - Stage 1

Answer

A

SBP 130-139 or DBP 80-89
Goal BP: <130/80

Risk <10% → Start w/ healthy lifestyle recommendations and reassess in 306 months

Risk >10% or known clinical cardiovascular ds (or diabetes, CKD) → Lifestyle recommendations and BP-lowering med

Question 63

Q

Guideline for the Prevention, Detection, Evaluation, and Management of High BP in Adults: HTN - Stage 2

Answer

A

SBP >140 or DBP >89
Goal: <130/80

Tx plan:
- Lifestyle changes and BP-lowering meds (two meds of different classes)
- reassess BP in 1 month
- If goal is met after 1 month, reassess in 3-6 months
- If goal not met after 1 month, consider different medications or titration
- Continue monthly follow-up until BP control is achieved

Question 64

Q

Guideline for the Prevention, Detection, Evaluation, and Management of High BP in Adults: Lifestyle modifications

Answer

A

FIRST-line therapy for HTN, HLD, DM2
- Lose weight if overweight
* BMI 25-29.9 or obese BMI >30
* Normal BMI: 18.5 0 24.9
- Stop smoking
- Reduce stress level
- Reduce dietary sodium: <1.5 g/day (1,500 mg/d)
- Maintain adequate dietary intake of potassium (>3,500 mg/day) in pts w/ normal kidney fx
- Limit alcohol intake
- Eat fatty cold-water fish (salmon, anchovy) 3x/week

Answer 65

A

Men: 1 ounce (30 mL)
- up to 2 drinks or less daily

Women: 0.5 ounce (15 mL)
- up to one drink or less daily

Answer 66

A

Recommended for preHTN, HTN, and weight loss

Goal: Eat foods rich in potassium, magnesium, and calcium
- Reduce red meat and processed foods
- Eat more whole grains and legumes
- Eat more fish and poultry
- Diet is high in fruits and vegetables
- has mod low-fat diary
- low in animal protein

Grains: 7-8 daily servings
Fruits and vegetables: 4-5 daily servings
Nuts, seeds, and dry bears: 4-5 servings per week
Fats, oils, or fat-free dairy products: 2-3 daily servings
Meat, poultry, and fish: <2 daily servings
Sweets: try to limit to fewer than 5 servings/week
Avoid high-sodium foods: cold cuts, ready-made foods, any pickled foods (cucumbers, eggs, pork parks)

Answer 67

A

Calcium → low-fat dairy
Potassium → most fruits and vegetables
Magnesium → dried beans, whole grains, nuts
Omega-3 oils → anchovy, krill, salmon, flaxseed

Answer 68

A

All diuretics will ↓ blood volume, venous pressure, and preload (cardiac filling)
Effect is antagonized by NSAIDs
Monitor electrolytes, esp Na and K

Answer 69

A

Controls BP by inhibiting reabsorption of Na and Cl ions in distal tubules of kidneys
- have favorable effect w/ osteopenia/osteoporosis (slows down demineralization) by slowing down calcium excretion by kidneys
  - Can cause photosensitivity reaction (avoid tanning)
  - all thiazides contain sulfa compounds; avoid if pt has sulfa allergy
“Hyper”
- Hyperglycemia (careful w/ diabetes)
- Hyperuricemia (can precipitate a gout attack; contraindicated in gout)
- Hypertriglyceridemia and hypercholesteremia (check lipid profile)

“Hypo”
- Hypokalemia (potentiates digoxin toxicity, ↑ risk of arrhythmias)
- hyponatremia (hold diuretic, restrict water intake, replace K loss)
- hypomagnesemia

- Gout
  - Hypotension
  - Hypokalemia
  - Renal failure
  - Lithium treatment
  - Sensitivity to sulfa drugs and thiazides
- Hydrochlorothiazide 12.5 25 mg PO daily
  - Chlorthalidone (Hygroton) 12.5 to 25 mg PO daily
  - Indapamide (Lozol) PO daily
  - Chlorothiazide (Diuril) daily or divided dose

Answer 70

A

Inhibit the Na-K-Cl pump of the kidney in the loop of Henle

2.

- Hypokalemia (potentiates digoxin toxicity; increases risk of arrhythmias)
  - hyponatremia (hold diuretic, restrict water intake, replace K loss)
  - hypomagnesemia
  - possibly altered excretion of lithium and salicylates
- Anuria (kidney failure)
  - Sensitivity to loop diuretics
- Furosemide (Lasix) PO BID
  - Bumetanide (Bumex) PO BID

Answer 71

A

If sulfa allergies, may have cross-sensitivity to thiazides and loop diuretics

Other drugs w/ sulfa:
- sulfonylureas
- sulfa antibiotics
- sulfasalazine
- some protease inhibitors (darunavir, fosamprenavir)
- may also be sensitive to topical sulfas (ophthalmic drops) or topical silver sulfadiazine (Silvadene)

Answer 72

A

Spironolactone antagonizes action of aldosterone → ↑ elimination of water in kidneys and conserves potassium
* Drug class: mineralocorticoid receptor antagonists or antimineralocorticoids
- Resistant HTN
  - HF
  - Hirsutism
  - Acene
  - Precocious puberty
  - Primary aldosteronism
- Gynecomastia, galactorrhea
  - Hyperkalemia
  - GI: vomiting, diarrhea, stomach cramps
  - postmenopausal bleeding
  - erectile dysfunction
- Hyperkalemia (serum K >5.5 mEq/L)
  - Renal insufficiency (serum creatinine >2.0 mg/dL in men; >1.8 mg/dL in women)
  - DM2 w/ microalbuminuria
- Spironolactone (Aldactone) daily
  - Eplerenone (Inspra) daily

Answer 73

A

Binds w/ beta-receptors on the heart and peripheral blood vessels; ↓ vasomotor activity; ↓ CO; inhibits renin (kidneys) and norepinephrine release
- 2 types of beta-receptors: B1 (cardiac effects) and B2 (e.g., lungs, vascular smooth muscle)
** Avoid abrupt discontinuation after chronic use; wean slowly; may precipitate angina and MI
See notecard
- Asthma, COPD, chronic bronchitis, emphysema (chronic lung ds)
  * 2nd/3rd heart block (fine to use w/ 1º heart block)
  * Sinus bradycardia
- Beta-blockers: ends w/ -olol

Cardioselective beta-blockers (B1 receptors):
- Atenolol (Tenormin)
- Metoprolol (Lopressor)
- Bisoprolol

Nonselective beta-blockers (inhibits both B1 and B2 receptors):
- Propranolol (Inderal)
- Timolol
- Pindolol

** Some beta-blockers have both alpha- and beta-blocking action: Labetalol (Normodyne) and carvedilol

Answer 74

A

Labetalol (Normodyne) and carvedilol

Answer 75

A

- Acute MI: ↓ mortality during acute MI and post-MI
  - Migraine headache: for prophylaxis only (not for acute attacks)
  - Glaucoma: ↓ intraocular pressure (Betimol ophthalmic drops for open-angle glaucoma)
  - Resting tachycardia (target HR <100 bpms)
  - Post-MI: ↓ mortality
  - Hyperthyroidism/thyroid storm and pheochromocytoma: Controls sx until primary ds is treated
  - Essential tremor: treat sx w/ nonselective beta-blocker propranolol

Answer 76

A

Blocks voltage-gated calcium channels in cardiac smooth muscle and the blood vessels → systemic vasodilation
- Nondihydropyridines → less potent vasodilators but have greater depressive effect on cardiac conduction and contractility (negative inotropic effect)
- Dihydropyridines → more potent vasodilators w/ little to no negative impact on contractility or conduction
- HTN
  - Angina
  - Arrhythmias
- Headaches (d/t vasodilation)
  - ankle edema (from vasodilation; benign)
  - heart block or bradycardia (depresses cardiac muscle and AV node)
  - Reflex tachycardia (seen w/ dihydropyridines [ex: nifedipine])
- 2nd/3rd degree heart block (fine to use w/ 1st degree)
  - Bradycardia
  - CHF
Dihydropyridine CCBs (-pine ending):
- Nifedipine (Procardia XL) daily
- Amlodipine (Norvasc) daily
- Felodipine (Plendil) daily

Nondihydropyridine CCBs
- Verapamil (Calan SR) daily or BID
- Diltiazem (Cardizem CD) daily

Answer 77

A

ACEi = inhibit activity of angiotensin-converting enzyme → ↓ conversion of angiotensin I to II (more potent vasocontrictor)

ARB = block the effect of angiotensin II

Preferred drugs (monotherapy or combined w/ other drug classes) for diabetes, CKD, congestive HFrEF, and after MI, esp. those w/ HF or reduced systolic fx
*** Pregnancy Category C (First Trimester) and Category D (Second and Third Trimesters) ► Fetal kidney malformations, fetal hypotension, fetal death
- Dry hacking cough (up to 10% w/ ACEis; less w/ ARBs)
  - Hyperkalemia, angioedema (rare, but may be life-threatening)
- Mod-severe kidney disease
  - Renal artery stenosis →
  * precipitates ARF
  * Hyperkalemia; also a SE, will have additive effect
ACEIs
- Ramipril (Altace) daily in 1-2 divided doses
- Benazepril (Lotensin) daily initially
- Enalapril (Vasotext) daily in 1-2 divided doses
- Fosinopril (Monopril) daily

ARBs
- Losartan (Cozaar) daily in 1-2 divided doses
- Candesartan (Atacand) daily in 1-2 divided doses
- Olmesartan (Benicar) daily in 1-2 diveded doses
- Irbesartan (Avapro) daily

Combination antihypertensive drugs: ACEIs OR ARBs (not both together) are combine dw/ other drug classes such as CCBs or thiazide duiretics

Answer 78

A

Potent vasodilators; relax smooth muscle found on bladder neck, prostate gland, and relieves obstructive voiding sx such as weak urinary stream, urgency, and nocturia
AKA alpha-adrenergic blockers
- suffix of -zosin
  - give at HS, very low doses; slowly titrate up
  - Tell pt to get out of bed slowly to prevent postural hypotension
  ** Not a first-choice for HTN except for men w/ both HTN and BPH
- Dizziness and hypotension (postural)
  - “First-dose orthostatic hypotension” is common (warn pt)
  - may cause severe hypotension and reflex tachycardia

4.

- Terazosin (Hytrin): HTN and BPH (starting dose 1 mg PO HS)
  - Doxazosin (Cardura): HTN and BPH
  - Tamsulosin (Flomax): BPH only

Answer 79

A

Inhibits RAS by blocking renin
- ↓ renin activity by ~75%
Do NOT combine aliskiren w/ ACEi or ARB → higher risk of hyperkalemia

3.

4.

- Aliskiren (Tecturna) daily
  - Aliskiren and hydrochlorothiazide daily

Answer 80

A

Combination of neprilysin inhibitor (sacubitril) w/ ARB (valsartan)
*New drug class for treatment of HFrEF
Sacubitril/valsartan (Entresto)

Answer 81

A

- Benazepril
  - Enalapril
  - Lisinopril
  - Ramipril
- Dry cough (5-20%; more common in females)
  - Angioedema
  - Hyperkalemia

Careful w/ CKD, renovascular ds
Do NOT use during pregnancy
Careful when using w/ potassium-sparing diuretics (e.g., triamterene, spironolactone) d/t ↑ risk of hyperkalemia

Answer 82

A

- Candesartan
  - Losartan
  - Valsartan
  - Irbesartan
- Hyperkalemia
  * Do NOT use during pregnancy

Answer 83

A

- Sacubitril w/ valsartan (Entresto)
- Hypotension
  - Hyperkalemia
  - Cough
  - Angioedema

Answer 84

A

- Verapamil
  - Diltiazem
- Heart block
  - Bradycardia
  - Constipation

Answer 85

A

- Amlodipine
  - Felodipine
  - Nicardipine
  - Long-acting nifedipine
  - Nisoldipine
- Headache
  - Flushing
  - tachycardia
  - Pedal EDema

short-acting nifedipine and nicardipine causes reflex tachycardia; NOT recommended for HTN

Answer 86

A

Beta-selective: atenolol, metoprolol

Non-beta selective: Propranolol, nadolol

Alpha-beta blockade: Carvedilol, labetalol

- Bradycardia
  - Fatigue
  - Insomnia
  - Erectile Dysfunction
  - Bronchospasm (asthma, COPD)

Answer 87

A

- Hydrochlorothiazide
  - Chlorthalidone
  - Indapamide
- Hypokalemia
  - hyponatremia
  - hyperuricemia
  - hypercalcemia
  - dehydration

Women w/ osteopenia/osteoporosis should receive this; helps bone loss by slowing down Cas loss (from bone) and stimulating osteoclasts

Answer 88

A

- Furosemide
  - Bumetanide
  - Torsemide
- Hypokalemia
  - hyponatremia
  - hyperuricemia
  - dehydration

Answer 89

A

- Triamterene
  - Amiloride

Aldosterone antagonists:
- Spironolactone
- eplerenone

- Hyperkalemia
  - hyponatremia
  - dehydration

Answer 90

A

- Doxazosin
  - Prazosin
  - Terazosin
- Orthostatic hypotension

Answer 91

A

At least 2 meds; can initiate w/ one or two antihypertensive meds (combined or two separate agents)
Diuretics, ARNI, ACEI or single-agent ARB, BB
ACEI or ARB as first line
- African Americans are less sensitive to ACEIs and ARBs; if BP still elevated, combine w/ dihydropyridine CCB or thiazide diuretic
ARB or ACEi as first line
- can add CCBs or thiazides or another drug class
Thiazides or CCBs may be more effective
BB, ACEi, aldosterone

Answer 92

A

EF <40% → HFrEF, aka systolic HF
EF >40% → HFpEF, diastolic HF

Causes:
- acute MI
- CAD
- HTN
- Fluid retention
- valvular abnormalities
- arrhythmias

- Crackles, bibasilar rales (rales on LL of lungs)
  - cough
  - dyspnea
  - ↓ breath sounds
  - dullness to percussion
- JVD: normal JVD is 4cm or less
  - Enlarged spleen and enlarged liver → anorexia, nausea, and abdominal pain
  - LW edema w/ cool skin

S/S of both LV and RV failure
- paroxysmal nocturnal dyspnea
- orthopnea
- nocturnal nonproductive cough
- wheezing (cardiac asthma)
- HTN
- fatigue

- S3 gallop, can be accompanied by anasarca
  * S3 heart sound is a sign of HR; although it can be heard in pregnant women and children/young adults

Answer 93

A

severe generalized edema d/t effusion of fluid into extracellular space

Answer 94

A

- CXR → increased heart size (cardiomegaly), interstitial and alveolar edema, Kerley B lines, and other signs of pulmonary edema
  - EKG, creatine phosphokinase (CPK), cardiac troponins (Troponin I, Troponin T)
  - B-type natriuretic peptide (BNP), N-terminal pro-BNP (NT-proBNP); both ↑ w/ HF but renal failure/CKD can also elevate these 2 labs
  - BUN and creatinine, electrolytes, CBC, LFTs
  - ECHO w/ Doppler flow study
  - Weight should be checked daily to detect fluid accumulation

Answer 95

A

- Acute decompensated HF → Refer to ED (IV furosemide, oxygen, vasodilators_
  - Diuretic (typically loop diuretic) → used to relieve sx of volume overload (dyspnea, peripheral edema) in primary care
  - Stabilize HFrEF → Combination tx w/ diuretic, ACEi or ARB, or ARNI, and BB
  - Limit Na intake
  - Pts w/ HF are best managed by cardiologist or at a heart clinic
  - Use BB if HFrEF (carvedilol, bisoprolol, extended-release metoprolol succinate)
  ► start with very low dose
  ► careful w/ initial dosing; can worsen
  ► consult or refer to experienced heart clinic
  ► started after the pt has been initiated on ACEI/ARB/or ARNI
  - Use New York Heart Association (NYHA) system to classify pt’s degree of cardiac disability
  - Refer to cardiologist; if in distress → Refer to ED!

First line of treatment for stable HF: ACEi or ARB

Answer 96

A

Class I → No limitations on physical activity
Class II → Ordinary physical activity results in fatigue, exertional dyspnea
Class III → Marked limitation in physical activity
Class IV → Symptoms are present at rest, with or without physical activity

Answer 97

A

Restrict or abstain from alcohol
smoking cessation if smoker
weight loss
Restrict Na to 2-3 g/d
Fluid restriction (1.5-2L/d) may help some pts

Answer 98

A

Both left and lung start with “L” → symptoms are lung related → dyspnea, orthopnea, and paroxysmal nocturnal dyspnea

Right-sided HF sx are GI related → anorexia, nausea, and RUQ abdominal pain

Answer 99

A

Thrombi develop inside deep venous system of legs or pelvis 2º to stasis, trauma to vessel walls, inflammation, or ↑ coagulation; PE is considered another manifestation of this thromboembolic ds

Etiology: 3 categories
- Stasis: Prolonged travel/inactivity (>3 hrs), bed rest, CHF
- Inherited coagulation ds: factor C deficiency, Leiden, etc
- ↑ coagulation d/t external factors: OC use, pregnancy, bone fractures esp of long bones, trauma, recent surgery, malignancy

- gradual onset of swelling on a LE after hx of travel (>3 hrs), prolonged sitting/inactivity
  - painful and swollen LE → red and warm
  - If PE → accompanied by abrupt onset of chest pain, dyspnea, dizziness, or syncope
  *Many pts are asymptomatic

Unprovoked DVT: No identifiable environmental cause
Provoked DVT: Caused by known event (e.g., surgery, major surgery >30 mins, hospitalization)

Answer 100

A

- Homan’s sign
  - CBC, platelets, clotting time (PT/PTT/INR), D-dimer level, CXR, EKG
  - US (whole legs or proximal leg)
Hospital admission
- Low-molecular-weight heparin SubQ or IV, then warfarin (Coumadin) PO
- or initial episode duration of tx w/ DOACs for at least 3 months
- For recurrent DVT or elderly, antithrombotic tx may last a lifetime
- PE, death
  - Stroke, and other embolic episodes

Answer 101

A

Lower leg pain on dorsiflexion of the foot (low sensitivity)

Answer 102

A

Inflammation of superficial vein d/t local trauma
- Higher risk if indwelling catheters, IV drugs (e.g., potassium), 2º bacterial infection (S. aureus)
- Some pts may have coexistent DVT)
- acute onset of an indurated vein (localized redness, swelling, and tenderness)
  - usually located on extremities
  - pt is afebrile w/ normal VS

PE
- Indurated cord-like vein that is warm and tender to touch w/ surrounding area of erythema
- No swelling/edema of the entire limb (think of DVT)

- NSAIDs (ibuprofen or naproxen Na) BID
  - Warm compresses
  - elevated limb
  - If septic cause → admit to hospital

Answer 103

A

Gradual (decades) narrowing and/or occlusion of medium-to-large arteries in LE. Blood flow to extremities gradually ↓ over time → permanent ischemic damage (gangrene of toes/foot)
- Higher risk: HTN, smoking, diabetes, HLD
- Previously known as peripheral vascular disease
- older pt w/ hx of smoking and HLD
  - worsening pain w/ ambulation (intermittent claudication) → instantly relieved by rest
  - over time, sx worsen until pt’s walking distance is greatly impaired
  - atrophic skin changes
  - some have gangrene on ≥1 toe(s)
Skin: atrophic changes → shiny and hyperpigmented ankles, hairless, cool to touch; gangrene of toes

Cardiovascular: ↓-to-absent dorsal pedal pulsese (may include popliteal and posterior tibial pulse); ↑ capillary refill time (<2 sec); bruits over partially blocked arteries

Answer 104

A

Ankle-brachial index (ABI) used to evaluate severity of PAD
- ≤0.9 → diagnostic for PAD
- ≤0.5 → severe arterial disease
→ Refer to vascular specialist

ABI 0.91 - 1.3 is normal

- SBP of ankle and arm (brachial) is checked after being in supine for 10 min using BP cuff and US probe
  - ABI score is done for each ankle

To measure ABI: Divide highest SBP (measure each arm and choose the higher BP) by the highest SBP of each ankle

Answer 105

A

- Smoking cessation (smoking causes vasoconstriction)
  - daily ambulation exercises
  - Pentoxifylline (Trental) if indicated, but effect is marginal (compared with cilostazol)
  - Cilostazol (Pletal)
  - Percutaneous angioplasty or surgery for severe cases
- Gangrene of foot and/or LE w/ amputation
  - ↑ risk of CAD
  - ↑ risk of carotid plaquing (check for carotid bruits)

Answer 106

A

a phosphodiesterase inhibitor ( direct vasodilator)
- can be taken with aspirin or clopidogrel
- Grapefruit juice, diltiazem, and omeprazole can ↑ serum concentration if taken together

To treat PAD.

Answer 107

A

Reversible vasospasm of peripheral arterioles on fingers and toes to an exaggerated response to cold temperature or emotional stress
- Unknown cause
- Associated w/ ↑ risk of autoimmune disorders (e.g., thyroid disorder, pernicious anemia, RA)
- Most are females (60-90%); gender ratio 8:1
- Pt w/ no underlying disease have “primary” Raynauds
- Secondary Raynauds occur in pts w/ concurrent autoimmune ds (e.g., SLE, scleroderma)
- Spontaneous remission may occur

To evaluation: check distal pulses, ischemic signs (ischemic ulcers on fingers/toes)

- middle-aged woman c/o chronic and recurrent episodes of color changes on fingers in a symmetric pattern (both hands and feet)
  - colors range from white (pallor) to blue (cyanosis) to red (reperfusion)
  - numbness and tingling
  - attacks lasts for several hours
  - hands and feet become numb w/ very cold temperatures
  - some have livedo reticularis
  - Ischemic changes may be present after a severe episode such as shallow ulcers (eventually heal) on some of the fingertips
- Avoid touching cold objects and being in cold water
  - avoid stimulants (e.g., caffeine)
  - maintain whole body warmth
  - use thermal underwear, layered clothing, hat, gloves/mittens, and hand warmers
  - smoking cessation is important
  - TX: CCBs → nifedipine (Adalat) or amlodipine (Norvasc)
  - Do not use any vasoconstricting drugs (e.g., Imitrex, ergots, pseudoephedrine/decongestants, amphetamines) or diet pills
  - avoid nonselective beta-blocker
- Small ulcers on fingers and toes

** Think of the colors of the American flag as a reminder for this disorder

Answer 108

A

violaceous mottling or reticular pattern of skin of the arms and legs

Answer 109

A

- Presentation range from full-blown d9sease to subacute endocarditis
  - common pathogens:
  * Gram+ (e.g., viridans streptococcus, S. aureus)
  - AKA IE
  - Parenteral antibacterial tx for native valve endocarditis can range4 from 4-6 weeks
- adult male w/ fevers
  - chills
  - malaise
  - a/w subungual hemorrhages
  - Osler’s nodes
  - Janeway lesions
  - may have heart murmur
  - may not present w/ all preceding sx

Look for cardiac risk factors
prosthetic valve
hx of valvular or congenital heart ds
cardiac device
IVD, IV lines
recent dental/surgical procedure
** Maintain high suspicion d/t high mortality

- Refer to cardiologist/ED for hospitalization/IV abx
  - BC x3 (first 24 hours)
  - CBC (↑ WBCs)
  - sedimentation rate >20 mm/hr (↑)
- Valvular destruction
  - myocardial abscess
  - emboli
  - death

Answer 110

A

- Mitral valve prolapse (unless hx of bacterial endocarditis)
  - GU/GI incisions/invasive procedures (except if existing infection present [e.g., UTI before cystoscopy])
High-risk Conditions
- previous hx of bacterial endocarditis
- prosthetic heart valves including homograft, valvular repair
- unpaired (or repaired) cyanotic congenital heart ds
- cardiac transplant w/ valvopathy

Invasive Procedures
- Dental procedures that traumatize oral mucosa, gingiva, or the periapical area of teeth, such as routine dental cleaning, tooth extractions, dental abscess drainage
- Invasive procedures on respiratory tract (esp. if tissue is infected); only if procedure involves incision or biopsy

Amoxicillin 2 g PO x 1 dose (adults)
If PCN allergy: clindamycin 600 mg or clarithromycin (Biaxin) 500 mg or cephalexin (Keflex) 2 g

Answer 111

A

splinter hemorrhages on nails

Answer 112

A

- Classing finding: midsystolic click w/ late systolic murmur
  - Common cause for mitral regurgitation
  - At higher risk for AF, thromboemboli, TIA, AF, and ruptured chordae tendinae

Best diagnostic: 3D-TEE

Mitral valve prolapse syndrome: Pt w/ sx and MVP

- Tall, thin adult female c/o fatigue
  - palpitations
  - lightheadedness (orthostatic hypotension) aggravated by heavy exertion
  - dyspnea
  - dizziness
  - exercise intolerance
  - panic
  - anxiety ds
  - may be asymptomatic
  * R/o Marfan’s syndrome if pt w/ pectus excavatum, hypermobility of joints, and arm span > height
- Asymptomatic → Does NOT need treatment; MVP usually benign
  - MVP w/ palpitations → BB
  * Avoid caffeine and stimulants, alcohol, cigarettes; ↓ stress
  - Echocardiography recommended for pt w/ clinical exam suggestive of MVP or those w/ family hx of MVP

Answer 113

A

- Elevated lipids
  - Most are asymptomatic until ASCVD; score using ASCVD; may underestimate 10-year and lifetime risk for some race/ethic groups such as American Indians, some Asians (e.g., South Asians), and some Hispanics (e.g., Puerto Ricans)
- USPSTF: screening in both men and women at an increased risk for coronary heart disease
  - Men ≥35 yo
  - Females ≥45 yo
  - Adults ≥76 w/ no hx of CVD: do NOT screen (insufficient evidence)
Risk Factors: Heart disease
- HTN
- Fam hx of premature heart disease (women w/ MI before 65 years; men w/ MI before 55 years)
- DM (considered a CHD risk equivalent even if pt has no hx of preexisting heart ds)
- Dyslipidemia
- Low HDL-C (<40 mg/dL)
- Age (Men >45; women >55)
- Cigarette smoking
- Obesity (BMI ≥30 kg/m2)
- Microalbuminuria
- Carotid artery disease
- Peripheral vascular disease (PVD)

Answer 114

A

Normal: <200 mg/dL
Borderline high: 201 - 239 mg/dL
High: >240 mg/dL

Answer 115

A

M: >40 mg/dL
F: >50 mg/dL

HDL > 60 mg/dL → associated w/ lower risk of heart disease
HDL <40 mg/dL → associated w/ ↑ risk of CAD even if normal LDL or cholesterol
- Genetic causes is probably most common reason for low HDL-C

Do NOT treat low HDL-C alone (aim for lowering LDL); clinical trials have not shown a correlation b/w raising HDL-C and ↓ rates of heart disease or stroke

Meds ↑ HDL
- fibrates (gemfibrozil)
- niacin
- some high-dose statins
** Although niacin can ↑ HDL (and ↓ triglycerides), it has fallen out of favor d/t having failed to reduce vascular events (stroke, ASCVD); low-dose niacin (vit B3) OTC multivitamins or B-complex vitamins have not been implicated

Lifestyle modifications:
- regular, moderate cardiovascular/aerobic exercises most days of the week
- lose weight
- eat health fats (salmon, tuna, nuts)
- eliminate transfats
- stop smoking

Answer 116

A

Optimal: <100 mg/dL
LDL: <130 mg/dL for low-risk pts w/ fewer than 2 RF
Heart disease or diabetes: <70 mg/dL

Answer 117

A

Normal: <150 mg/dL
Hypertriglyceridemia: >150 mg/dL
* Niacin and fibrates are best agents for ↓ triglycerides
- Very high levels can be d/t genetic (primary) and acquired (secondary) ds; both often coexists
  - Metabolic syndrome
  - DM
  - familial hypertriglyceridemia
  - alcohol abuse
  - hyperthyroidism
  - kidney disease
  - medications (e.g., anabolic steroids, Accutane)

Meds that can ↑ triglycerides
- Oral estrogens
- diuretics
- Second-gen antipsychotics
- glucocorticoids
- antiretroviral
- tamoxifen
- Isotretinoin
- nonselective BB (e.g., propranolol)

≥1,000 mg/dL
- Avoid alcohol if very high triglycerides, can precipitate acute pancreatitis; avoid alcohol and acetaminophen (hepatoxic use)
  - Identify case, such as certain meds and past med hx
  - treat triglycerides first if very high (before tx high LDL/cholesterol)
  - First-line meds: fibrates (fenofibrate [Tricor], gemfibrozil [Lopid], benzafibrate [Bazalip])
  - Niacin (Vit B3) high dose can ↓ triglyceride by 40% and raise HDL by 40%; start at low dose, take aftr meal, and slowly ↑ dose
  * To tx niacin flush or “prickly heat” sensation (from vasodilation), take w/ aspirin
  - High doses of strong statins such as atorvastatin (Lipitor) and rosuvastatin (Crestor) can ↓ triglycerides (33-50%)
  - Marine omega-3 acid ethyl esters are also effective (Lovaza 4 g/day)
- ↓ sugar and simple carb (junk food)
  - avoid alcoholic drinks
  - follow low-fat diet
  - eat fish w/ omega-3 (Salmon, sardines) twice a week
  - lose weight; reduce simple carbs, sugars, and junk foods, fried foods
  - ↑ aerobic-type physical activity

** If pt has markedly high triglycerides (≥500 mg/dL), lower triglycerides FIRST (niacin or fibrate) before treating high cholesterol and LDL; very HIGH triglycerides ↑ risk of acute pancreatitis

Answer 118

A

Mediterranean diet
DASH diet
vegetarian diet
low-carbohydrate diet
low trans-fatty acid diet

Answer 119

A

First line: lifestyle changes
- weight loss
- exercise most days of the week
- diet low in saturated fat
- smoking cessation
- in the presence of ASCVD and other factors → initiate statin therapy w/ lifestyle changes
- Reduce dietary salt intake and + DASH diet (low salt, low saturated fat <30%)
- Encourage use of soluble fiber in diet (e.g., inulin, guar gum, fruit, vegetables) to enhance lowering LDL (lowers LDL by blocking absorption in GI tract up to 10%)
- Target goal is to lower LDL first (except if very high triglyceride levels)
- If high triglycerides (≥500 mg/dL), treat hypertriglyceridemia first d/t high risk of acute pancreatitis
- Low HDL alone (even if normal LDL and cholesterol) is a risk factor for heart disease

Answer 120

A

recent coronary syndrome (within past 12m)
Hx of MI
hx of ischemic stroke
Symptomatic PAD (hx of claudication w/ ABI <0.85 or previous revascularization or lower extremity emputation)

Answer 121

A

High Intensity Statin
- Clinical ASCVD
- Very high risk ASCVD*
- Severe primary hypercholesteremia w/ LDL >190 mg/dL
- Diabetic age 50-75 yrs w/ LDL > 70 mg/dL

Moderate Intensity Statin
- Diabetic age 40-75 years w/ LDL >70 mg/dL
- Age 40-75 yo w/ 10-year ASCVD risk >7.5% w/ risk-enhancing factors
- Age 40-75 yo w/ 10-year ASCVD risk 7.5-19.9% w/ risk-enhancing factors

Defined as hx of multiple major ASCVD events or one major ASCVD event w/ multiple high-risk conditions

Answer 122

A

High-Intensity Statins: Lowers LDL ≥50%
- Atorvastatin (Lipitor) 40-80 mg/d*
- Rosuvastatin (Crestor) 20-40 mg/d

Initiation at 80 mg/d is not recommended by the FDA; increases risk for myopathy/rhabdomyolysis; start at lower dose and titrate up to 80 mg (if tolerated)

Moderate-Intensity Statins: Lowers LDL 30-50%
- Atorvastatin 10-20 mg/d
- Rosuvastatin (Crestor) 5-10 mg/d
- Simvastatin (Zocor) 20-40 mg/d
- Pravastatin (Pravachol) 40-80 mg/d
- Lovastatin (Mevacor) 40 mg/d

Low-Intensity Statins: Lowers LDL <30%
- Simvastatin 10 mg/d
- Pravastatin 10-20 mg/d
- Lovastatin 20 mg/d
- Fluvastatin 20-40 mg/d

Answer 123

A

Age ≥ 65 years

Cardiovascular
- Hx of prior CABG, PCI, CHF, HTN

Endocrine
- DM

Resp
- Current smoker

Kidney
- CKD (eGFR 15-59 mL/min)

Lipids
- Persistently elevated LDL of ≥100 mg/dL despite statin therapy and ezetimibe

Answer 124

A

Patients w/ any form of clinical ASCVD (hx of MI, CAD, angina, stroke/TIA, PAD, coronary revascularization)
→ High-intensity statin (or max tolerated statin therapy)
→ ↓ LDL by 50%

High-intensity Statins: * Memorize
- adult 21-75 years w/ any type of ASCVD (e.g., CAD, PAD, stroke, TIA) is given high-intensity statins such as atorvastatin 40-80 mg or rosuvastatin 20-40 mg
- adult w/ LDL >190 mg/dL (w/out ASCVD or DM) is a candidate for high-intensity statin dosing

Very high risk of ASCVD (defined as hx of multiple major ASCVD events or one major ASCVD event w/ multiple high-risk conditions):
→ High-intensity statin
→ LDL goal is 70 mg/dL
→ If already on high-intensity dose of statin and not at goal (LDL 70 mg/dL), add a nonstatin such as ezetimibe/Zetia
→If on statin and ezetimibe (LDL remains >70 mg/dL), adding a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor is reasonable (although long-term safety >3yrs is unknown)

Diabetic [t /w LDL of ≥70 mg/dL:
→ 40-75 yrs: Moderate-intensity statin therapy (w/out calculating 10-year ASCVD risk)
→ 50-75 yrs: Can use high-intensity statin to ↓ LDL by 50% or more

Severe primary hypercholesterolemia (LDL of 190 mg/dL or higher):
- 20-75 years: High-intensity statin (w/out calculating 10-year ASCVD risk)
- If on high-intensity statin and LDL ≥100 mg/dL, add ezetimibe (Zetia)
- If multiple risk factors for ASCVD, consider adding a PCSK9 inhibitor to statin

Assess adherence and percentage response to LDL-lowering meds and lifestyle changes:
- Repeat lipid in 4-12 weeks after statin initiation or dose adjustment
- Repeat Q3-12 months PRN

Answer 125

A

If 10-year ASCVD risk of 7.5-19.9% (intermediate risk):
- 40-75 years w/ LDL 70 mg/dL to 189 mg/dL (without DM) → Assess risk-enhancing factors for ASCVD; if decision to start statins uncertain, check the coronary artery calcium (CAC) score; if CAC score is 1-99, favor starting statin therapy

If 10-year ASCVD risk ≥20% (high risk):
- 20-38 years w/ LDL ≥160 mg/dL (without DM) → If positive fam hx or premature ASCVD, initiate statin therapy to ↓ LDL by 50%

Answer 126

A

R/o familial hypercholesterolemia (FH), if presence of extensor tendon xanthomas 9achilles, subpatellar, or hand extensor tendons)

Answer 127

A

Family hx of premature ASCVD
Persistently elevated LDL-C levels of ≥160 mg/dL
Metabolic syndrome
CKD
Hx of preeclampsia or premature menopause (age <40 years)
High-risk ethnic groups such as South Asians (from India, Pakistan, Sri Lanka, Nepal, Bangladesh)
Chronic inflammatory disorders (e.g., psoriasis, RA, or chronic)
Persistent triglyceride elevations
Elevated C-reactive protein of ≥2.0 mg/L
ABI ≤0.9

Answer 128

A

HMG-CoA reductase: enzyme in liver that is responsible for cholesterol synthesis. Statins inhibit this enzyme, which results in ↓ lipoprotein production
- Best at lowering LDL, and some can ↑ HDL and ↓ triglycerides at higher doses

If pt is a high-intensity statin candidate, start at lower doses and titrate up slowly to the recommended dose to minimize adverse effect
- Check baseline LFT before initiation
- Some pts may not tolerate high-intensity statins (e.g., muscle pains, weakness) but can tolerate moderate-intensity statins
- If pt at very high risk for ASCVD or has severe primary hypercholesteremia (LDL >190 mg/dL) and is NOT ta LDL goal (but already on high-dose statin), next step is to add ezetimibe (Zetia) to statin
- If still not at goal (LDL 70 mg/dL), can add a PCSK9 inhibitor (Repatha, Proluent) to statin and ezetimibe

Examples:
- Pravastatin (Pravachol)
- Lovastatin (Mevacor)
- Simvastatin (Zocor)
- Atorvastatin (Lipitor)
- Rosuvastatin

** Simvastatin and lovastatin drug interactions (high risk of rhabdomyolysis):
- Avoid grapefruit juice
- Fibrates
- Antifungals (itraconazole, ketoconazole)
- Macrolides (erythromycin, clarithromycin, telithromycin)
- Amiodarone (Cordarone), some CCBs (diltiazem, amlodipine, verapamil)

** May cause cognitive effects (e.g., memory loss, confusion); reversible upon discontinuation of statin therapy (brain and nerves are mostly fat)

Combination regimens of a statin w/ ezetimibe (Zetia) is acceptable for some high-risk patients

Answer 129

A

Niacin (OTC) daily or TID
Niaspan (slow-release niacin) daily
Avoid combining niacin w/ statins (higher risk of liver damage)
Adding niacin to statins has NOT been shown to produce further benefit but may increase risk of hepatotoxicity

Answer 130

A

Gemfibrozil (Lopid)
Fenofibrate (Tricor)
Benzafibrate (Bezalip)
Do not use w/ severe renal disease

Action: Reduces production of triglycerides by liver and increases production of HDL
- Very good agents for lowering triglycerides and elevating HDL levels
- Less effective at lowering LDLs compared w/ statins

SE:
- dyspepsia
- gallstones
- myopathy

Answer 131

A

Cholestyramine (Questran Light)
Colestipol (Colestid)
Colesevelam (Welchol)

Action: Works locally in small intestine; interfere w/ fat absorption, including fat-soluble vitamins (vit a, D, E, and K)

Alternative rug for pts who cannot tolerate statins, fibrates, and niacin

If used alone, not as effective as statins in lowering LDL; no hepatotoxicity

SE: Mainly GI
- Bloating
- flatulence
- abdominal pain

Start at lose dose and titrate up slowly.
* Advise pt to take multivitamin tablets daily

Answer 132

A

Ezetimibe (Zetia)

Action: Absorbs cholesterol from small intestines; combination of a statin w/ ezetimibe recommended for some high-risk ASCVD pts

Contraindications:
- active liver disease
- unexplained persistent elevation of ALT and AST

can be taken alone or combined w/ a statin or fibrate (e.g., simvastatin [Vytorin])

SE:
- diarrhea
- joint pains
- tiredness

Answer 133

A

Human monoclonal antibodies, can ↓ LDL by 50-60%
Reduction of risk for MI, stroke, and unstable angina
Can be used aone or w/ other lipid-lowering therapies (statins, ezetimibe)
SubQ Q2-4 wks

Current guidelines:
- add PCSK9 to statins for pts at very high risk of ASCVD, recent ACS (within 12 m), multiple MIs, or strokes

Ex:
- Evolocumab (Repatha)
- Alirocumab (Praluent)

Answer 134

A

Acute breakdown and necrosis of skeletal muscle (myoglobins) will cause acute renal failure
- >50% of pts do not report muscular sx
- muscles involved are usually the thighs, calves, shoulders, and lower back
- Higher doses of statins or combination therapy have higher risk
* R/o rhabdo if pt on statin and complains of muscular pain w/ dark-colored urine
Triad of:
- muscle pain (myalgia)
- weakness
- red-to-brown urine
order labs immediately!
- Creatine kinase (if markedly elevated; at least 5x the upper limit of normal from 1,500 to >100,000 IU/L)
- Urine: Reddish-brown color (myoglobinuria) and proteinuria in up to 45% LFTs (will be elevated)
- Other labs: UA, BUN, creatinine, potassium/electrolytes, EKG
Discontinue statin immediately

Answer 135

A

splinter hemorrhages on nails

Answer 136

A

red macules on palms/soles, not painful (may be tender)

Answer 137

A

painful/tender violaceous (violet-color) nodes found mostly on pads of fingers/toes, thenar eminence

Answer 138

A

- > 1/3 (39.6%) adults are obese
  * M: 38.0%, F: 41.4%
  - Non-Hispanic Blacks have highest rates of obesity (48.1%), then Hispanics (42.5%), and non-Hispanic Whites (34.5%)
  - Among obese, 40.2% are middle-age adults (40-59 yrs)

Obesity increases risk of mortality and comorbidities:
- DM 2, HTN, dyslipidemia, CHD, sleep apnea, and ↓ mobility

The “apple-shaped” body type is considered more dangerous for health compared to the “pear-shaped” body type

Answer 139

A

<18.5 - Underweight
18.5-24.9 - Normal weight
25-29.9 - Overweight
30-39.9 - Obese
>40 - Grossly obese

** BMI 27 is overweight → initiate lifestyle education

Answer 140

A

M: >40 inches (102 cm)
South Asians, >35 inches (90 cm)

F: >35 inches (88 cm)
South Asians, >31 inches (80 cm)

Answer 141

A

M: 1.0 or higher
F: 0.8 or higher

Answer 142

A

Weight loss w/ dietary therapy and lifestyle and behavioral modifications
Many dietary methods (e.g., Weight Watchers, keto, Nutrisystem, Atkins) and apps (e.g., Noom, Weight Watchers) that help promote weight loss; depends on pt preferences
Meal delivery services can deliver fresh meals to homes; makes cooking easier d/t provided ingredients (e.g., Blue Apron, Hello Fresh, Green Chef)
Exercise: 40 mins of moderate to vigorous physical activity at least 3-5x/week
Walking 10,000 steps daily is popular; use of smart watches that track steps and exercise is helpful
Many online social support group sites, blogs, and articles about weight loss

Therapies not recommended:
- liposuction (does not improve insulin sensitivity or risk factors for heart ds)
- herbal dietary supplements
- very low-calorie diets (<1,000 kcal/day)

Answer 143

A

Metabolic ds w/ cluster of sx; pts at higher risk for DM2, CVD, and stroke; AKA insulin resistance syndrome or syndrome X
At least 3/5 must be present to diagnose:
- Abdominal obesity (>40 inches in men; >35 inches in women)
- BP >130/85 mmHg
- ↑ fasting plasma glucose (>100 mg/dL(
- ↑ triglycerides (>150 mg/dL) or on drug tx for ↑ triglycerides
- ↓ HDL (<40 mg/dL in men; <50 mg/dL in women)
** Caused by hyperinsulinemia and peripheral insulin resistance
- Fasting (9-12 hrs) lipid profile (esp. triglycerides and HDL)
  - Fasting BG
  - Weight (BMI), waist circumference, BP

Answer 144

A

- caused by triglyceride fat deposits (steatosis) in liver hepatocytes
  - most asymptomatic
  - can present w/ or w/out inflammation
  - common in Western industrialized countries
  - most common reason: chronic heavy alcohol consumption and obesity (w/ DM2 and/or w/ metabolic syndrome)

RF:
- central obesity
- DM2
- metabolic syndrome

- Usually asymptomatic
  - May have hepatomeglay
  - annual PE will show mild-to-mod elevations of ALT and AST
  - if sx → fatigue, malaise, w/ vague RUQ pain
  - associated dw/ obesity, metabolic syndrome, DM, and hyperlipidemia
- LFT: ALT and AST may be slightly ↑ from 2-5x the upper limit of normal; normal transaminase levels do NOT exclude NAFLD
  - Fasting lipid levels, glucose, A1C
  - Order hepatitis A, B, and C profile
  - Initial imaging test is liver US and HAFLD fibrosis score
  - Refer to GI for management and a liver biopsy (GOLD STANDARD!)

** NAFLD is a/w metabolic syndrome and/or obesity; look for slightly elevated ALT and AST (not related to alcohol or meds) and negative Hep A, B, and C

- Lose weight, exercise, and watch diet
  - D/c alcohol intake permanently
  - Avoid hepatotoxic drugs (e.g., acetaminophen, isoniazid, statins)
  - Recommend vaccination for hepatitis A, B, and annual flu vaccine
  - Refer to GI specialist
- All obese and overweight pts should be advised to lose weight (esp. diabetics)
  - lifestyle changes are important! (diet, nutrition, exercise, portion control)
  - Daily aerobic exercise (e.g., walking, swimming, biking) for 30-40 mins
  - Weight Watchers: Some pts like the support and education (tertiary prevention)

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Cardiovascular Flashcards

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