Final Exam :( Flashcards by Zach Bell

group of conditions that includes nonobstructive and obstructive coronary artery disease with or without previous myocardial infarction, ischemic heart disease, chronic angina syndromes

chronic coronary disease (CCD)

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caused by narrowing in major coronary arteries that supply blood to the heart that is mostly the result of atherosclerotic plaques, comes from imbalance between myocardial oxygen supply and demand, common clinical manifestations include chronic stable angina, unstable angina, MIs

ischemic heart disease (IHD)

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what is the most common symptom of ischemic heart disease (IHD)?

angina

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smoking, elevated LDL/total cholesterol, diabetes, HTN, obesity, overconsumption of alcohol, age (over 45 for men, over 55 for women), gender, family history

major risk factors for ischemic heart disease (IHD)

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______ has established atherosclerotic plaque in coronary arteries that gets in the way of coronary blood flow whereas _______ has atherosclerotic plaque rupture with subsequent clot formation

stable ischemic heart disease (IHD), acute coronary syndrome (ACS)

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form of angina that comes from spasm/vasoconstriction of a coronary artery without significant atherosclerosis

prinzmetal or variant angina

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class of angina where patient is able to perform ordinary physical activity without any symptoms but prolonged exertion leads to symptoms

class I

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class of angina where symptoms sort of limit ordinary physical activity, walking rapidly or longer time, climbing more than one flight of stairs causes symptoms

class II

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class of angina where symptoms more significantly limit ordinary physical activity, walking less than 2 blocks or one flight of stairs causes symptoms

class III

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class of angina where angina may occur at rest, any physical activity causes symptoms

class IV

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when medical therapy isn’t working, symptoms are unstable, or there is extensive coronary atherosclerosis then _______ is performed in ischemic heart disease patients

percutaneous coronary intervention (PCI)

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______ is performed when patients are found to have extensive coronary atherosclerosis or medical treatment isn’t working

CABG surgery

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general treatment recommendations for stable ischemic heart disease: first lifestyle modifications and potentially ________, then providers will go to low dose _______ or _____ if the first is contraindicated, then treatment moves to potentially adding _______ or ______ if the patient has preexisting conditions, then there could be triple therapy with _______, _______, and _______/______

immediate release nitrate, aspirin, clopidogrel, ACEi, ARBs, beta blockers, CCBs, long acting nitrate/ranolazine

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recommendation for antiplatelet therapy in chronic coronary disease (CCD) with no indication for anticoagulation

low dose aspirin for at least 12 months if not longer

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recommendation for antiplatelet therapy in PCI patients

dual antiplatelet therapy or drug eluting stent for 6 months then single antiplatelet therapy after that

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recommendation for antiplatelet therapy in PCI and high bleeding risk

drug eluting stent and dual antiplatelet therapy for 1-3 months, then P2Y12 inhibitor for 9 months, then single antiplatelet therapy thereafter

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recommendation for antiplatelet therapy in PCI with indication for anticoagulation

direct oral anticoagulant (DOAC)/clopidogrel/aspirin for 1 month, then DOAC and clopidogrel for 6 months, then DOAC alone thereafter

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why is dual antiplatelet therapy required after stent placement?

stents are prone to producing blood clots until they become covered in endothelial cells like a normal coronary artery so DAPT is required until stent is covered in endothelial cells

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patients who have not experienced bleeding complications on DAPT or not at high risk of bleeding should be considered for _______ (prolonged/shorter) duration of DAPT

prolonged

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patients with significant bleeding complications or at high risk of this are generally considered for _______ (prolonged/shorter) duration DAPT

shorter

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which drugs for angina work through decreasing myocardial oxygen demand?

beta blockers, CCBs, ranolazine

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which drugs for angina work by increasing myocardial arterial blood supply?

CCBs and nitrates

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what drugs are first line therapy for long term prevention of angina symptoms?

beta blockers

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if angina symptoms are not improved with first line agent what is recommended?

CCBs

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this drug is often given to patients with angina that doesn't respond to other medications, use when patient already has low baseline BP or HR since it has little effect on BP and HR

ranolazine

this type of beta blocker should be avoided as antianginal agents because they have partial beta agonist effects and cause lesser reductions in HR at rest creating less reductions in myocardial oxygen demand

intrinsic sympathomimetic activity (ISA) - acebutolol, pindolol, labetalol

this type of CCBs are typically more effective antianginal agents because they slow down node conduction in the heart, decrease HR, and further decrease the myocardial oxygen demand

non-dihydropyridine CCBs (cardioprotective) - verapamil, diltiazem

the combination of beta blocker and _______ CCBS is preferred because they might improve symptoms better than either drug alone (beta blocker prevents reflex increases in sympathetic tone and HR and this type of CCB will have potent vasodilatory effects)

dihydropyridines - amlodipine, nifedipine, felodipine

can long acting nitrates be used as monotherapy and why?

no because tolerance occurs with continued use of nitrates so there will have to be a nitrate free period of time for the patient leaving the patient unprotected

these agents are NOT preferred in variant angina because they can worsen vasospasm due to unopposed alpha receptor stimulation

beta blockers

these agents are preferred in variant angina

CCBs and nitrates

occurs when the heart doesn't pump enough blood to meet the blood flow and metabolic demands of the body and is usually a result of low cardiac output

heart failure

_______ is the fraction of volume present at the end of diastole that gets pushed in the aorta during systole, systolic dysfunction (HFrEF) is characterized by a left ventricular ejection fraction (LVEF) of ______ or less whereas diastolic dysfunction (HFpEF) is characterized by a LVEF of _____ or greater and the heart has impaired ventricular filling

ejection fraction, 40%, 50%

volume of blood ejected per unit of time = HR x SV

cardiac output

ventricular filling pressure at the end of diastole, related to the volume of blood in left ventricle just prior to systole, determined by venous return/ventricular relaxation/atrial contraction

preload

resistance to ventricular ejection, regulated by ejection impedance/wall tension/geometry, elevated aortic/systemic pressures create an increase in this and reduced stroke volume

afterload

with sudden decrease in CO the body responds by increasing blood volume and prioritizing blood flow to vital organs like heart and brain, because of this there is decreased renal perfusion which starts the renin-angiotensin-aldosterone system (RAAS) which produces angiotensin II and there is a synthesis and release of aldosterone, aldosterone then stimulates Na+ and water retention which increases intravascular volume and therefore preload so in a failing heart changes in contractile filaments decrease the ability of the heart muscle cells to adapt to these increases in preload so this increase in preload can further impair contractile function and CO

preload and Frank-Starling compensatory mechanisms in HF

increase in HR is a way to increase CO especially when contractility is reduced which happens due to sympathetic nervous system activation and agonist effect of NE on heart beta-adrenergic receptors, because SV is fixed in HF tachycardia is a big determinant of CO, however this response increases heart muscle oxygen demand/worsens ischemia/contributes to proarrhythmia/further impairs systolic and diastolic function

tachycardia and increased afterload compensatory mechanisms in HF

________ is an adaptation to a change in wall stress and is regulated by neurohormonal activation (angiotensin II and aldosterone major stimuli for this), changes in heart muscle and extracellular matrix composition/function that causes structural and functional changes in the heart, however in HF these changes are detrimental to heart function

cardiac remodeling

_______ is an increase in ventricular muscle mass due to growth of myocytes, happens because of an increase in volume or pressure, concentric (in response to pressure overload) or eccentric (happens after acute MI) hypertrophy, component of cardiac remodeling, can reduce the wall stress in short term but long term can increase myocyte death through increase in oxygen demand, major contributor to diastolic dysfunction

ventricular hypertrophy

this sided HF is characterized by systemic congestion symptoms like peripheral edema, GI bloating, fatigue

right

this sided HF is characterized by pulmonary symptoms like dyspnea (SOB, difficulty breathing), orthopnea (SOB, difficulty breathing when lying down), nocturnal dyspnea (sudden episodes of SOB that occur at night when patient is sleeping)

left

HTN, atherosclerotic cardiovascular disease, diabetes, metabolic syndrome, obesity, exposure to cardiotoxic agents, genetic variant for cardiomyopathy, positive family history of cardiomyopathy

risk factors for developing HF

recommendation for stage B HF patients with LVEF less than/equal to 40% is _______ or _______, for stage B with recent MI and LVEF less than/equal to 40% is _________, LVEF less than/equal to 30% greater than 1 year survival greater than 40 days post MI is ________

ACEi, beta blocker, ARB is ACEi intolerant, ICD

recommendation for stage C HF patients is ______ in NYHA II-II/_______ or _______ in NYHA II-IV, along with ________, __________, and ________ (last one as needed)

ARNi, ACEi, ARB, beta blocker, MRA, SGLT2i, diuretics

which drugs in the following classes should be used in HFrEF stage C/D treatment? RAASi, beta blocker, MRA, SGLT2i

RAASi - ARNi like Entresto, ACEi when ARNi not feasible, ARB when neither are feasible BB - bisoprolol, carvedilol, metoprolol succinate MRA - spironolactone or eplerenone SGLT2i - dapagliflozin or empagliflozin

how often should guideline directed medical therapy (GDMT) be titrated to target doses?

every 1-2 weeks

______ are used to relieve acute symptoms of congestion and maintenance of euvolemia (state of having normal amounts of blood/fluids in the body), ________ are preferred because they continue to have an effect even when patient has reduced renal function

diuretics, loop diuretics

the maximum response to loop diuretics that can be seen in chronic HF patients is reduced creating a _______ dose, doses above this have limited added benefit, can increase the frequence to 2-3 times a day dosing or combining loop diuretic with a thiazide diuretic

ceiling

an ARNi should not be administered concomitantly with an ACEi or ARB within how many hours of the last dose of the ACEi or ARB?

36 hours

what labs need to be monitored with MRAs, frequency?

eGFR, serum potassium, should be monitored at initiation, after 1 week, after 4 weeks, then every 6 months

what agents should be maximized prior to addition of ivabradine? what does ivabradine decrease?

beta blockers, HR

__________ (increase/decrease) in cardiovascular death of HF hospitalizations was seen with addition of vericiguat?

decrease

non-dihydropyridine CCBs, antiarrhythmics and dronedarone, thiazolidinediones, DPP-4 inhibitors (saxagliptin, alogliptin), NSAIDs should all be avoided in what patients due to potential to cause harm?

HF patients

age (risk doubles with each decade after 50), history of VTE, venous stasis, vascular injury, hypercoagulable state, drug therapy (estrogen containing OC, estrogen replacement therapy, SERMs, heparin, chemotherapy)

risk factors for VTE

what type of VTE risk factors are present within 3 months before VTE diagnosis, surgery with general anesthesia for greater than 30 minutes, confinement to bed in hospital for at least 3 days with acute illness, C section, major trauma

major transient risk factors

what type of VTE risk factors are present within 2 months before VTE diagnosis, surgery with general anesthesia for less than 30 minutes, admission to hospital for less than 3 days with acute illness, estrogen therapy, pregnancy, confinement to bed out of hospital for at least 3 days with acute illness, leg injury associated with reduced mobility for at least 3 days, prolonged car/air travel

minor transient risk factors

S/S of this include unilateral leg pain on the affected leg, swelling after night's sleep, cyanosis of the skin in affected leg, post-thrombotic syndrome (PTS, long term complication of DVT caused by damage to venous valves which produces chronic lower extremity swelling pain, tenderness, skin discoloration/ulceration)

DVT

S/S of this include shortness of breath, tachycardia, coughing blood

this test can confirm if a patient does NOT have DVT, measures fibrin breakdown in the serum and is a marker of acute thrombotic activity, these tests are not specific markers for VTE, but a negative test can be used to rule out DVT diagnosis

D-dimer test

the Padua prediction score is used to predict VTE for _________ patients and a score of ___ or more indicates high risk of VTE, the Caprini risk assessment score is used to predict VTE for _________ patients and a score of ____ or more indicates high risk of VTE, patients with moderate to high risk should receive pharmacologic prophylaxis

hospitalized medical, 4, general surgical, 5

prophylaxis for VTE patients that have undergone knee/hip replacement/repair should continue for a duration of a minimum of ______ days but extending it to _____ days is recommended due to the continued VTE risk up to 1 month post-surgery

10-14, 35

this type of drug decreases short term pain and swelling and prevents destruction of venous valves, these drugs can be used for patients with pulmonary embolism with shock, hypotension, or massive DVT with limb gangrene, they are controversial because compared with anticoagulants they restore venous potency more quickly, but the bleeding risk associated with the use of this type of drugs is significantly higher

thrombolytics

_________ should have the following dosing for VTE: 100 mg infused over 2 hours, near the end or immediately following the infusion a PARENTERAL anticoagulant should be started, this should be done when aPPT or thrombin time returns to twice normal or less

alteplase (tPA)

_______ will not dissolve a formed clot like thrombolytics, but they prevent the clot's propagation (movement towards the heart) and growth in VTE

anticoagulants

in patients with VTE the guidelines recommend apixaban, dabigatran, edoxaban, or rivaroxaban over __________

vitamin K antagonist (warfarin)

if a patient has a GI malignancy, _______ and ______ had a higher risk of GI major bleeding than LMWH but _______ does not so LMWH or this option may be preferred in patients with GI malignancies

edoxaban, rivaroxaban, apixaban

the recommendation for patients with antiphospholipid syndrome is adjusted dose _________ with a target INR of 2.5 over DOAC therapy

vitamin K antagonist (warfarin)

phase of anticoagulation for VTE, initial anticoagulants following VTE diagnosis, parenteral or high dose oral anticoagulation lasting 5-21 days depending on anticoagulant regimen

initiation phase

phase of anticoagulation for VTE, period after initiation following which treatment is completed for acute VTE event, anticoagulants used at standard therapeutic doses and is considered complete after 12 weeks of anticoagulation

treatment phase

phase of anticoagulation for VTE, use of anticoagulants at full or reduced dose for secondary prevention (reducing risk of recurrent VTE events in the future), no preplanned stop date for this phase

extended phase

what is the recommended duration of treatment phase for patients with an acute VTE without any contraindications

3 months

what phase of anticoagulation therapy should be offered in patients with VTE diagnosed in the setting of a major transient risk factor? what agents and dosing strategy is preferred in this phase?

extended phase, reduced dose apixaban or rivaroxaban

during warfarin initiation, INR monitoring should happen ________ for hospitalized patients and every _______ for nonhospitalized patients. after initiation, INR should be monitored every ______ days during the first week of therapy then once a week for the first 1-2 weeks, then every 2 weeks, and eventually ________ thereafter

daily, 1-3 days, 2-3 days, monthly

what factors cause patient specific variations in dosing requirements for warfarin and fluctuation in INR?

hepatic metabolism, genotype differences, diet, drug-drug interactions, health status

chaotic rapid (300-500 bpm) and irregular atrial rhythm, results from electrophysiological abnormalities that are part of impulse generation or structural abnormalities of cellular connections that normally facilitate rapid/uniform impulse conduction, also comes from waves of electrical activity coming from ectopic action potentials from pulmonary veins in left atrium or in response to interstitial fibrosis, patients can be asymptomatic or have fatigue, palpitations, dizziness, lightheadedness, dyspnea (SOB) chest pain if underlying CAD is present, near-syncope and syncope, can feel “heart beating fast” or “fluttering” or “beat out of my chest”

a fib

if a patient with a fib is hemodynamically unstable what is the recommended treatment for acute RATE control?

direct current cardioversion (electrical shock to restore normal heart rhythm)

if a patient with a fib is hemodynamically stable and does not have decompensated HF, what is the recommended treatment for acute RATE control?

beta blockers/verapamil/diltiazem, then digoxin, then amiodarone

if a patient with a fib has LVEF less than/equal to 40% what is the recommended treatment for long term RATE control and what is contraindicated?

beta blockers recommended, non-dihydropyridine CCBs (diltiazem/verapamil) are contraindicated due to potential of exacerbating HF

if a patient with a fib has LVEF greater than 40% what is the recommended treatment for long term RATE control?

beta blockers OR non-dihydropyridine CCBs

what resting HR should be targeted with rate control therapies for a fib?

less than 100 bpm, up to 110 bpm

caution should be taken with _______ because of the risk of chemical cardioversion (alter the rhythm of the heart) so patients should be anticoagulated or evaluated by echocardiography to rule out blood clots before use

amiodarone

these drugs slow atrial conduction velocity/prolong refractoriness which interrupts reentrant circuits and restores sinus rhythm

drugs for rhythm control

direct current cardioversion is generally _____ (more/less) effective than drug therapy for converting atrial fibrillation to sinus rhythm

in patients experiencing a fib episode of ______ hours or longer conversion to sinus rhythm should be deferred unless known that an atrial thrombus is not present

for delayed cardioversion, anticoagulation should be utilized for greater than/equal to ______ weeks prior and ______ weeks after cardioversion

3, 4

in early cardioversion, start IV _____, SC _______, or oral _______

heparin, LMWH, DOAC

possible significant adverse reactions with this drug include hypotension, hepatotoxicity, proarrhythmic effects, pulmonary toxicity, thyroid effects

amiodarone

rate and rhythm control strategies have ________ clinical outcomes in many patients with a fib

comparable

_______ control is preferred over ______ in a fib and the nonpreferred strategy should only be initiated in patients with paroxysmal a fib who continue to experience symptoms despite maximum tolerated doses of preferred drugs

rate, rhythm

_________ therapy is important for patients with a fib because it can prevent stroke and systemic thromboembolism

anticoagulation

what does the CHA2DS2-VASc score stand for?

congestive heart failure hypertension age greater than/equal to 75 years (2 points) diabetes stroke, TIA, thromboembolism history (2 points) vascular disease (prior MI, PAD, aortic plaque) age (65-74 years) score (maximum 9 points)

what do the different CHA2DS2-VASc scores indicate?

0 men/1 women - may omit anticoagulation 1 men/2 women - oral anticoagulation may be considered 2+ men/3+ women - oral anticoagulation recommended

in patients with rheumatic mitral stenosis or mitral stenosis of moderate or greater severity and history of a fib, which is preferred for long term anticoagulation, DOACs or warfarin?

warfarin

a fib dosing for apixaban

5 mg BID unless patient is older than 80, body weight less than 60 kg, serum creatinine greater than 1.5 - reduce dose to 2.5 mg BID

a fib dosing for rivaroxaban

20 mg once daily with evening meal

a fib dosing for dabigatran

150 mg BID

a fib dosing for warfarin

5 mg once daily for most patients

abrupt development of focal neurological deficit that occurs due to inadequate blood supply to an area of the brain, can be thrombotic or embolic

ischemic stroke

result of bleeding into the brain and other spaces within the central nervous system and includes subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH), and subdural hematomas

hemorrhagic stroke

short episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction, rapid onset and short duration typically lasting less than 30 minutes to 1 hour, no deficit remains after this

transient ischemic attack (TIA)

when is aspirin NOT recommended for primary prevention of stroke?

patients with diabetes, asymptomatic peripheral arterial disease, low risk

all patients should have a ______ or _______ to differentiate and ischemic stroke from a hemorrhagic stroke because the treatment for each differs, fibrinolytic therapy must be avoided until hemorrhagic stroke is ruled out

brain CT, MRI scan

_______ should not generally be treated in the acute period of an ischemic stroke because it may cause decreased blood flow to the ischemic areas which may increase the infarction size, may be necessary to treat in patients with severely elevated BP who are otherwise candidates for fibrinolytic therapy, patients with stroke and other medical disorders like aortic aneurysm rupture, MI, HF

hypertension

inclusion criteria for use of alteplase in ischemic stroke

18 or older, clinical diagnosis of ischemic stroke causing a measurable neurological deficit, time of symptom onset well established to be less than 4.5 hours before treatment would begin

exclusion criteria for use in alteplase in ischemic stroke

nondisabling mild stroke (NIHSS 0-5), clinical presentation suggestive of SAH even with a normal head CT or intracranial hemorrhage on imaging, active internal bleeding, current oral anticoagulant use, current use of direct thrombin inhibitors or direct factor Xa inhibitors, previous intracranial hemorrhage

dosing of alteplase for patients who can be treated within 3 - 4.5 hours of symptoms of ischemic stroke onset

IV alteplase: 0.9 mg/kg with max dose at 90 mg over 60 minutes with initial 10% of dose given as a bolus over 1 minute

efficacy of ________ is measured by elimination of existing neurological deficits and long-term improvement in neurological status and functioning based on neurological examinations and other outcome measures

alteplase

when should a CT scan be obtained after IV infusion of alteplase before starting anticoagulants or antiplatelet agents?

24 hours after

in patients with minor noncardioembolic ischemic stroke that did NOT receive alteplase, guidelines recommend what type of antiplatelet therapy started within 24 hours after symptom onset and continued for 21 days

dual antiplatelet therapy (aspirin and clopidogrel)

what antiplatelet agents are recommended for secondary prevention of ischemic stroke?

aspirin, clopidogrel, or ER dipyridamole plus aspirin

when should anticoagulants be used for prevention of ischemic stroke?

in patients with a fib and previous TIA or stroke

why is management of BP after hemorrhagic stroke important?

prevent rebleeding and expansion of hematoma

what drug is recommended after SAH to prevent delayed cerebral ischemia? timeframe and dosing?

oral nimodipine, promptly after initial event but no later than 96 hours after SAH, 60 mg PO Q4H for 21 days

BP readings of systolic less than 120 AND diastolic less than 80

less than normal

BP readings of systolic 120-129 AND diastolic less than 80

elevated

BP readings of systolic 130-139 OR diastolic 80-89

stage 1 HTN

BP readings systolic greater than or equal to 140 OR diastolic greater than or equal to 90

stage 2 HTN

when do we initiate HTN treatment and recommended follow up times?

stage 1 HTN with clinical ASCVD or estimated 10-year risk greater than/equal to 10%, stage 2 HTN, reassess in 1 month

which BP agents are NOT recommended in patients with HFrEF?

CCBs

which BP agents are NOT preferred in patients with HFpEF?

aldosterone antagonists, CCBs, direct vasodilators

which BP agents are NOT recommended in patients with ischemic heart disease?

direct vasodilators

which BP agents should be used in patients with chronic kidney disease?

ACEi or ARB

which BP agents should be used in patients with postrenal transplant?

CCBs, ACEi

which BP agents are recommended for patients diabetes? what about diabetes and albuminuria?

diuretics, CCBs, ACEi/ARB for albuminuria

which BP agents should be used in secondary stroke prevention?

diuretics, ACEi, ARB

what BP agent should be used in a fib patients?

ARBs

when is it recommended to start therapy with two antihypertensive agents from different classes?

stage 2 HTN and average BP more than 20/10 above their BP target

which beta blockers are cardioselective (preferred in patients with asthma, COPD, peripheral vascular disease)?

atenolol, bisoprolol, metoprolol

beta blockers with vasodilatory properties

labetalol, carvedilol, nebivolol

patients failing to achieve goal BP despite adherence to optimal doses of three antihypertensive agents of different classes (ideally one being a diuretic) or those achieving goal BP on four or more antihypertensive agents have this and what can they be treated with?

resistant hypertension, hydralazine or minoxidil

severe elevations in BP (greater than 180/120 usually) and accompanied by acute or life threatening target organ damage, goal of therapy is to reduce systolic BP up to 25% in the first hour then lower to 160/100-110 over the next 2-6 hours, then carefully to normal over the following 24-48 hours

hypertensive emergency

severe elevation in systolic BP greater than 180 or diastolic greater than 110 without evidence of acute or life threatening target organ damage, can usually be managed by restarting or intensifying oral therapy

hypertensive urgency

antihypertensive therapy for pregnant patients and what should be discontinued

methyldopa, nifedipine, or labetalol should be used, ACEi or ARBs should be discontinued

starting age and interval at which patients should be screened for elevated cholesterol, which components should be tested?

all adults 20 years or older should be screened every 5 years using a fasting blood sample, total cholesterol, non-HDL, LDL, HDL, triglycerides

which lipid component is primary diagnostic and therapeutic target?

LDL

chronic kidney disease, hypothyroidism, obstructive liver disease/biliary cirrhosis

secondary causes of hyperlipidemia

1. established clinical ASCVD (secondary prevention) 2. elevation of LDL cholesterol levels 190 or higher (primary) 3. diabetes age 40-75 regardless of LDL cholesterol levels 4. without diabetes, age 40-75, with an estimated 10 year ASCVD risk of 7.5% or greater and LDL cholesterol 70-189

4 risk groups for statin treatment

patients between the ages of 40-75 who have cholesterol between 70-189, should be used to evaluate primary prevention, not secondary

group that requires ASCVD risk calculation

family history of premature ASCVD (male < 55, female < 65), primary hypercholesterolemia, metabolic syndrome, chronic kidney disease, chronic inflammatory conditions like psoriasis/RA/HIV/AIDS, history of premature menopause (before 40 years) and history of pregnancy associated conditions that increase later ASCVD risk (preeclampsia), high risk race/ethnicities (South Asian ancestry), lipid/biomarkers associated with increased ASCVD risk

risk enhancing factors for hyperlipidemia

coronary heart disease (MI, angina), cerebrovascular disease (stroke, TIA)

examples of clinical ASCVD

acute coronary syndrome, MI, ischemic stroke, peripheral arterial disease

major ASCVD events

- dietary cholesterol < 200 mg/day - saturated fats < 7% of total calories and reduce intake of trans fatty acids - therapeutic options for LDL-lowering plant stanols/sterols 2 g/day - increase viscous (soluble) fiber 10-25 g/day - total calories - adjust caloric intake to maintain desirable body weight and prevent weight gain - physical activity 150 min/week of moderate intensity or 75 min/week of vigorous intensity

examples of lifestyle changes that are recommended to reduce cardiovascular risk

- inhibitor of HMG-CoA reductase - 10-80 mg daily at any time of day, dose adjustment in renal dysfunction patients is not necessary - adverse effects: constipation, abdominal pain, diarrhea, nausea, myopathy (change therapy) - contraindications: acute liver failure, decompensated cirrhosis - monitoring: lipid panel, AST, ALT

atorvastatin

- inhibitor of HMG-CoA reductase - 20-40 mg as a single dose in the evening or 40 mg twice daily, 80 mg ER once daily, dose adjustment for mild to moderate renal impairment not necessary - adverse effects: constipation, abdominal pain, diarrhea, nausea, myopathy (change therapy) - contraindications: acute liver failure, decompensated cirrhosis - monitoring: lipid panel, AST, ALT

fluvastatin

- inhibitor of HMG-CoA reductase - 10-80 mg as a single dose with evening meal or divided twice daily with food, patients with severe renal insufficiency (CrCl above 30) dosages above 20 mg/day should be carefully considered and used cautiously - adverse effects: constipation, abdominal pain, diarrhea, nausea, myopathy (change therapy) - contraindications: active liver failure or decompensated cirrhosis, concomitant use of strong CYP3A4 inhibitors and erythromycin - monitoring: lipid panel, AST, ALT

lovastatin

- inhibitor of HMG-CoA reductase - 1-4 mg/day as a single dose that can be taken with or without food at any time of day, moderate renal impairment and end stage renal disease on hemodialysis should have starting dose of 1 mg daily (max 2 mg daily) - adverse effects: constipation, abdominal pain, diarrhea, nausea, myopathy (change therapy) - contraindications: active liver disease, decompensated cirrhosis, coadministration with cyclosporine, significant drug interactions - monitoring: lipid panel, AST, ALT

pitavastatin

- inhibitor of HMG-CoA reductase - 10-80 mg.day as a single dose at bedtime, significant renal or hepatic dysfunction starting dose of 10 mg daily recommended - adverse effects: constipation, abdominal pain, diarrhea, nausea, myopathy (change therapy) - contraindications: active liver disease, decompensated cirrhosis - monitoring: lipid panel, AST, ALT

pravastatin

- inhibitor of HMG-CoA reductase - 5-40 mg/day at any time of day, 40 mg reserved for those who do not achieve LDL cholesterol goal on 20 mg, renal dysfunction or Asian descent starting dose of 5 mg recommended - adverse effects: constipation, abdominal pain, diarrhea, nausea, myopathy (change therapy) - contraindications: active liver failure, decompensated cirrhosis - monitoring: lipid panel, AST, ALT

rosuvastatin

- inhibitor of HMG-CoA reductase - 5-40 mg/day as a single dose in the evening or divided, mild to moderate renal insufficiency dosage adjustment not necessary but caution should be used in patients with severe renal insufficiency (start at 5 mg daily and closely monitor), due to increased risk of myopathy use of 80 mg dose should be reserved for patients who have been taking it for greater than 12 months without muscle toxicity - adverse effects: constipation, abdominal pain, diarrhea, nausea, myopathy (change therapy) - contraindications: acute liver disease, decompensated cirrhosis, concomitant use of CYP3A4 inhibitors (select azole antifungals, select macrolide antibiotics, select HIV protease inhibitors, select hep C virus protease inhibitors), cyclosporine, gemfibrozil - monitoring: lipid panel, AST, ALT

simvastatin

- inhibits absorption of cholesterol at the brush border of small intestine, decreased delivery of cholesterol to the liver - 10 mg daily, no dosage adjustment necessary in patients with renal or mild hepatic insufficiency - adverse effects: increased serum transaminases and hepatotoxicity, myopathy - contraindications: significant drug interactions - monitoring: lipid panel, AST, ALT

ezetimibe

- forms nonabsorbable compex with bile acids in intestine releasing chloride ions in the process, inhibits enterohepatic reuptake of intestinal bile salts increasing fecal loss of LDLs - 4-24 g/day in two or more divided doses - adverse effects: nausea, constipation, bloating, flatulence, impairs absorption of fat-soluble vitamins - contraindications: complete biliary obstruction - monitoring: lipid profile

cholestyramine

- binds with bile acids in intestine to form insoluble complex that is eliminated in the feces, results in increased oxidation of cholesterol to bile acid lowering serum cholesterol - 3.75 g/day as single dose or divided twice daily with meals - adverse effects: nausea, constipation, bloating, flatulence, impairs absorption of fat soluble vitamins - contraindications: history of bowel obstruction, serum TG concentrations of more than 500 mg/dL, history of hypertriglyceridemia induced pancreatitis - monitoring: lipid profile

colesevelam

- binds with bile acids in intestine to form insoluble complex that is eliminated in feces, results in increased oxidation of cholesterol to bile acid lowering serum cholesterol - 5-30 g/day as single or divided dose - adverse effects: nausea, constipation, bloating, flatulence, impairs absorption of fat soluble vitamins - no contraindications - monitoring: lipid profile

colestipol

- may involve several actions including partial inhibition of release of free fatty acids from adipose tissue and increased lipoprotein lipase activity which may increase the rate of chylomicron triglyceride removal from plasma - ER is 1000-2000 mg daily at bedtime (use with caution in patients with renal impairment), IR is 1-6 g/day in two to three divided doses (do not exceed 6 g daily) - adverse effects: flushing, itching, gastric distress, headache, hepatotoxicity, hyperglycemia, hyperuricemia - contraindications: active hepatic disease or significant/unexplained persistent elevations in hepatic transaminases, active peptic ulcer, arterial hemorrhage - monitoring: blood glucose in patients with diabetes, if on concurrent statin then may periodically check CPK and serum potassium, liver function tests pretreatment, lipid profile, platelets, PT, uric acid, phosphorous

niacin ER and IR

- agonist for PPAR-alpha, increase in VLDL catabolism, fatty acid oxidation, elimination of triglyceride rich particles - 54-160 mg/day, dosage should be minimized in severe renal impairment - adverse effects: nausea, diarrhea, abdominal pain, rash, increased risk of rhabdomyolysis when given with statin, gallstones, myositis, hepatitis - contraindications: acute liver disease, biliary cirrhosis, persistent liver function abnormality, severe kidney impairment or end stage kidney disease, preexisting gallbladder disease, breastfeeding - monitoring: periodic blood counts during first year, lipid profile, LFTs, kidney function, S/S of myopathy

fenofibrate

- can inhibit lipolysis and decrease subsequent hepatic fatty acid uptake as well as inhibit hepatic secretion of VLDL, together these actions decrease serum VLDL levels and increase HDL - 1200 mg/day in two doses 30 minutes before meals, should be avoided in hepatic or severe renal impairment - adverse effects: nausea, diarrhea, abdominal pain, rash, increased risk of rhabdomyolysis when given with statin, gallstones, myositis, hepatitis - contraindications: hepatic or severe renal dysfunction, primary biliary cirrhosis, preexisting gallbladder disease, concurrent use with dasabuvir, repaglinide, simvastatin, significant drug interactions exist - monitoring: serum cholesterol, LFTs, CBC

gemfibrozil

- reduction in the hepatic production of triglyceride-rich very VLDLs - 4 g/day taken as a single dose or two 2 g doses daily - adverse effects: should be used in caution in patients with known hypersensitivity to fish/shellfish, dysgeusia (loss of taste), dyspepsia, eructation (burping) - no contraindications - monitoring: triglycerides and other lipids (LDL) should be monitored at baseline and periodically, ALT/AST

omega-3-ethyl esters

- reduction in the hepatic production of triglyceride rich VLDLs - 2 g twice daily with meals - adverse effects: should be used in caution in patients with known hypersensitivity to fish/shellfish, arthralgia - no contraindications - triglycerides and LDL monitored at baseline and periodically, hepatic impairment need to monitor ALT/AST, S/S of bleeding

icosapent ethyl

- human monoclonal antibody that binds to and inhibits PCSK9 which binds to LDL receptors on hepatocyte surfaces to promote downregulation of the receptors within the liver, this inhibition increases the number of LDL receptors available to clear LDL which lowers LDL levels - 75-150 mg once every 2 weeks SubQ injection or 300 mg once every month - adverse reactions: injection site reactions, nasopharyngitis, influenza, upper respiratory tract infections, urinary tract infections, elevation in liver enzymes - contraindications: hypersensitivity to the drug - monitoring: lipid profile, hypersensitivity reactions

alirocumab

- human monoclonal antibody that binds to and inhibits PCSK9 which binds to LDL receptors on hepatocyte surfaces to promote downregulation of the receptors within the liver, this inhibition increases the number of LDL receptors available to clear LDL which lowers LDL levels - 140 mg every 2 weeks or 420 mg once monthly subQ injection - adverse effects: injection site reactions, nasopharyngitis, influenza, upper respiratory tract infections, urinary tract infections, back pain - contraindications: hypersensitivity to drug - monitoring: lipid profile, monitor for hypersensitivity reactions

evolocumab

- adenosine triphosphate-citrate lyase (ACL) inhibitor that lowers LDL cholesterol by inhibiting cholesterol synthesis in the liver - 180 mg once daily, no dosage adjustments for patients with renal or hepatic insufficiency - adverse effects: hyperuricemia - contraindications: hypersensitivity to drug - monitoring: lipid levels, S/S of hyperuricemia, assess uric acid levels as clinically indicated, S/S of tendinopathy or tendon rupture

bempedoic acid

atorvastatin 40-80 rosuvastatin 20-40

high intensity statins (greater than/equal to 50% reduction)

atorvastatin 10-20 rosuvastatin 5-10 simvastatin 20-40 pravastatin 40-80 lovastatin 40-80 fluvastatin XL 80 fluvastatin 40 BID pitavastatin 1-4

moderate intensity statins (30-49% reduction)

simvastatin 10 pravastatin 10-20 lovastatin 20 fluvastatin 20-40

low intensity statins (less than 30% reduction)

what intensity statin is recommended for secondary prevention with history of multiple ASCVD events?

high intensity

what intensity statin is recommended for secondary prevention with history of 1 major ASCVD event + multiple high risk conditions?

high intensity

what intensity statin is recommended for primary prevention with LDL greater than or equal to 190?

high intensity

what intensity statin is recommended for primary preventionn with LDL 70-189 without diabetes (depends on ASCVD risk)?

ASCVD risk 7.5-20% and risk factors - moderate ASCVD risk greater than 20% - high

what intensity statin is recommended for primary prevention with LDL 70-189 with diabetes?

moderate intensity

when is ezetimibe used?

used primarily in combination with a statin when adequate reductions in cholesterol are not achieved or in patients who are statin intolerant

when are PCSK9 inhibitors used?

recommended to be added to maximum tolerated statin therapy in very high risk ASCVD patients

at what level are triglycerides addressed? what drug therapy options are recommended to treat elevated triglycerides?

above 500 mg/dL, niacin, fibrates, long chain omega-3 fatty acids

when should a repeat lipid panel be drawn?

4-12 weeks after initiation/titration and then every 3-12 months after that

when would it be recommended to reduce the dose of a statin?

muscle pain, liver enzyme abnormalities, kidney dysfunction

what components are used in the assessment of an overweight or obese patient?

BMI, waist circumference, body fat percentage, comorbidities, readiness to lose weight

BMI less than 18.5

underweight

BMI 18.5-24.9

normal weight

BMI 25-29.9

overweight

BMI 30-34.9

obesity class 1

BMI 35-39.9

obesity class 2

BMI greater than/equal to 40

extreme obesity class 3

high risk waist circumference for men and women?

greater than 40 inches in men, greater than 35 inches in women

CVD, type 2 diabetes, sleep apnea, cardiovascular risk factors (smoking, elevated LDL, decreased HDL, impaired fasting glucose)

comorbidities and risk factors that heighten the need for treatment of an overweight patient

what is the recommended initial weight loss goal and in what time frame should this occur?

5-10% weight loss, 1-2 lb per week meeting the initial weight loss goal within first 6 months of therapy

who is weight loss indicated for?

BMI of 25-29.9 with one or more indicators of increased CVD risk (elevated waist circumference, prediabetes, type 2 diabetes, HTN, dyslipidemia, current cigarette smoker) or for any patient with BMI greater than 30

anticonvulsants/mood stabilizers (carbamazepine, gabapentin, pregabalin, lithium), antidepressants (phenelzine, mirtazapine, citalopram, escitalopram, duloxetine), antidiabetics (insulin, glipizide, glyburide)

drug therapies that could contribute to weight gain

how many calories reduced equals one pound of weight loss?

500 calories

when should pharmacotherapy be initiated in addition to lifestyle modifications for weight loss?

BMI 27-29.9 with comorbidity or and BMI above 30

when should weight loss pharmacotherapy be discontinued?

weight will likely be regained if lifestyle changes/therapeutic interventions are not continued indefinitely

in which patients is bariatric surgery an option?

when other attempts have failed in severely obese patients (BI greater than 40 or greater than 35 with obesity related comorbidities)

what medication adjustments need to be considered after bariatric surgery?

crush tablets, open capsules, use liquids until appropriate to restart solid foods, avoid NSAIDs, diuretics, oral bisphosphonates, extended/delayed release products

- sympathomimetic amine, stimulation of the hypothalamus to release NE - 8-37.5 mg daily given in 1-3 divided doses - adverse effects: restlessness, tremor, palpitations/tachycardia, HTN, pulmonary HTN - contraindications: history of cardiovascular disease, hyperthyroidism, glaucoma, agitated states, history of drug abuse, MAO inhibitor within 14 days, pregnancy, breastfeeding - monitoring: weight and waist circumference every month for first 3 months, then at 3-month intervals

phentermine

- first drug is a sympathomimetic amine, stimulation of the hypothalamus to release NE, other drug blocks neuronal voltage-dependent sodium channels, enhances GABAA activity - 3.75/23 mg daily x 14 days, 7.5/46 mg daily x 12 weeks, titrate up to 11.25/69 mg daily x 14 days then 15/92 mg daily if first 12 weeks successful - adverse effects: constipation, paresthesia, xerostomia, blurred vision, impaired cognition, headache, kidney stones, increased upper respiratory tract infections, tachycardiac, metabolic acidosis - contraindications: hyperthyroidism, MAO inhibitor within 14 days, pregnancy, glaucoma - monitoring: weight, resting HR, serum potassium, glucose, creatinine, BP, mood disorders, glaucoma, dermatologic reactions

phentermine/topiramate

- reducing appetite appears to be secondary to CNS effects including stimulation of the hypothalamus to release NE - SHORT TERM THERAPY: IR 25 mg 3 times daily 1 hour before meals, CR 75 mg once daily midmorning - adverse effects: cardiac arrhythmias, ECG changes, HTN, palpitations, tachycardia, anxiety, depression, dizziness - contraindications: arteriosclerosis, severe HTN, hyperthyroidism, glaucoma, agitated states, history of drug abuse, MAO inhibitor within 14 days - monitoring: baseline cardiac evaluation, weight, waist circumference, BP, HR

diethylpropion

- SHORT TERM THERAPY: ER 105 mg once daily 30-60 minutes before morning meal, IR 17.5-35 mg 2-3 times daily 1 hour before meals - adverse effects: flushing, HTN, palpitations, tachycardia, agitation, dizziness, headache, insomnia - contraindications: glaucoma, pregnancy, highly nervous or agitated patients, history of drug abuse, hyperthyroidism, MAO inhibitor within 14 days - monitoring: baseline cardiac evaluation, weight, waist circumference, BP, HR

phendimetrazine

first drug is a pure opioid antagonist, second drug is a relatively weak inhibitor of the neuronal reuptake of dopamine and NE, may result from action on areas of the brain involved in regulation of food intake - LONG TERM THERAPY: tablets come as 8/90 mg daily x 1 week, increase as tolerated in weekly intervals, maximum dose 4 tabs/day - adverse effects: constipation, nausea, vomiting, headache, insomnia, sleep disturbances - contraindications: concomitant use of other products containing the drugs, chronic opioid, opiate agonist/partial agonist, acute opioid withdrawal, HTN, seizures, abrupt discontinuation of other drugs, MAO inhibitor within 14 days - monitoring: BP, HR, blood glucose, weight, BMI, renal and liver function, mental status for depression, suicidal ideation, anxiety

naltrexone/bupropion

- reversible inhibitor of gastric and pancreatic lipases thus inhibiting absorption of dietary fats by 30% - Rx is 120 mg TID with each main meal during or up to 1 hour after the meal, OTC is 60 mg 3 times daily with each main meal containing fat - adverse effects: vitamin deficiency, abdominal distress, abdominal pain, bowel urgency, frequent bowel movements, headache, back pain, infections - contraindications: pregnancy, chronic malabsorption syndrome, cholestasis - monitoring: BMI, weight, diet, serum glucose in patients with diabetes, LFTs in patients with hepatic impairment, renal function in patients at risk of renal impairment

orlistat

- long acting analog of human glucagon-like peptide-1 (GLP-1) which increases glucose dependent insulin secretion, decreases inappropriate glucagon secretion, increases B-cell growth and replication, slows gastric emptying, decreases food intake - LONG TERM, SC 0.6 mg once daily for 1 week, increase by 0.6 mg/day at weekly intervals to a target dose of 3 mg once daily - adverse effects: acute kidney injury, gallbladder disease, GI symptoms, medullary thyroid carcinoma, pancreatitis - contraindications: history/family history of medullary thyroid carcinoma, pregnancy - monitoring: plasma glucose, renal function, pancreatitis, triglycerides, gallbladder disease, suicidal thoughts/behaviors, HR, body weight

liraglutide

- selective glucagon-like peptide-1 (GLP-1) receptor agonist that increases glucose-dependent insulin secretion, decreases inappropriate glucagon secretion, slows gastric emptying; also acts in the areas of the brain involved in regulation of appetite and caloric intake - SC injection - 0.25 mg weekly for weeks 1-4 and titrate up every 4 weeks to maintenance dose of 2.4 mg weekly - adverse effects: acute kidney injury, gallbladder disease, GI symptoms, medullary thyroid carcinoma, pancreatitis - contraindications: history/family history of medullary thyroid carcinoma, patients with multiple endocrine neoplasia syndrome type 2 - monitoring: plasma glucose, heart rate, body weight, renal function, S/S of pancreatitis or gallbladder disease

semaglutide

- glucose-dependent insulinotropic polypeptide (GIP) receptor and glucagon-like peptide-1 (GLP-1) receptor agonist that increases glucose-dependent insulin secretion, decreases inappropriate glucagon secretion, slows gastric emptying, and decreases food intake (likely due to appetite mediation) - SC injection - 2.5 mg weekly for 4 weeks and titrate up every 4 weeks to a maximum weekly dose of 15 mg/week - adverse effects: acute kidney injury, gallbladder disease, GI symptoms, hypoglycemia, medullary thyroid carcinoma, pancreatitis - contraindications: history/family history of medullary thyroid carcinoma, patients with multiple endocrine neoplasia syndrome type 2 - monitoring: plasma glucose, GI adverse reactions, S/S of pancreatitis or gallbladder disease, emergence of worsening depression/suicidal thoughts or behaviors, changes in behavior, HR, body weight

tirzepatide

- production and release of thyroid hormones are regulated by this - TRH is synthesized in the neurons within the hypothalamus and is then carried to the pituitary - TRH activates the pituitary to synthesize and release TSH - TSH activates thyroid to stimulate the synthesis and secretion of thyroxine (T4) and triiodothyronine (T3) - T4 and T3 inhibit secretion of TSH which closes the feedback loop

hypothalamic-pituitary-thyroid axis

what is the preferred lab when monitoring patients with thyroid problems? target range?

TSH - highly sensitive biomarker of thyroid axis so changes in TSH are more easily seen, 0.5-4.5 mU/L

presence of these means that there is an autoimmune disorder in the patient and is often present in patients with hypothyroidism

anti-TPOAb

in what disease state is TSHR-SAb found?

Graves' disease

why are total T4 and total T3 not useful for assessing thyroid function?

high degree of protein binding of these hormones so the free fraction can be changed by the levels of binding proteins or degree of protein binding

chronic autoimmune thyroiditis (Hashimoto's disease), iatrogenic causes (irradiation, surgery), drugs (amiodarone, radiocontrast media, lithium, interferon alpha tyrosine kinase inhibitors, immune checkpoint inhibitors), transient thyroiditis (viral, postpartum), iodine deficiency/excess, thyroid gland infiltration (infection, malignancies, autoimmune, inflammatory)

primary causes of hypothyroidism

pituitary or hypothalamic diseases are examples of...

secondary causes of hypothyroidism

- fatigue, lethargy, sleepiness, mental impairment, depression, weight gain, menstrual disturbances, paresthesia, cold intolerance, change in voice, dry skin, decreased perspiration, decreased appetite, constipation, arthralgia, myalgia, infertility - slow movements, goiter, slow speech, hoarseness, bradycardia, anemia, dry skin, weight gain, non-pitting edema, hyporeflexia, delayed relaxation of reflexes

hypothyroidism signs and symptoms

why is LT4 the treatment of choice for almost all hypothyroid patients?

LT4 mimics the normal physiology of the thyroid gland which secretes mostly T4 as a prohormone and peripheral tissues convert T4 to T3 as they need it based on metabolic demands

content: synthetic LT4 gold standard for treating hypothyroidism

levothyroxine

content: synthetic T3 rarely needed in treatment of hypothyroidism, no outcome benefit to combining with LT4

liothyronine

content: dessicated pork thyroid glands, contains T3 and T4 non-physiologic T4:T3 ratio, no advantage over LT4 monotherapy

dessicated thyroid (Armour)

how do the pharmacokinetics differ in LT4 and T3?

LT4 has pharmacokinetic advantages over T3, LT4 has a 7-10 day half-life so little peak and trough effect on dose-response curve making LT4 the preferred choice over T3 UNLESS patient has impairment of conversion of T4 to T3 then addition of T3 may be necessary

TRUE/FALSE: patients should be maintained on the same LT4 product which can be done by prescribing name brand without allowing substitution

TRUE

patients with long term _______ (over/under) treatment of hypothyroidism are at risk for atrial fibrillation and other cardiovascular morbidities, anxiety, depression, osteoporosis

over

patients with long term _____ (over/under) treatment of hypothyroidism are at risk for hypercholesterolemia and other cardiovascular problems, depression, obstetric complications

under

how might the coadministration of calcium and iron change the way you counsel a patient on their use of LT4?

LT4 has greatest and most consistent bioavailability when taken in evening on empty stomach, patients should take LT4 dose at least 2 hours before or 6 hours after calcium or iron dose

what factors may alter LT4 dose requirements?

aging, weight loss, drugs/dietary factors, increased thyroxine-binding globulin (TBG) due to cirrhosis, estrogen therapy, increased clearance, critical illness

what is the recommended interval for general monitoring of TSH for hypothyroidism? following a dose change?

monitor serum TSH every 6-12 months or if any change in clinical status, 6-8 weeks after any dose or product change, as soon as possible in pregnancy then monthly

any syndrome resulting from excess thyroid hormone

thyrotoxicosis

related to excess thyroid hormone production and secretion by the thyroid gland

hyperthyroidism

most common cause of hyperthyroidism in non-elderly adults

Graves' disease

Graves' disease, toxic multinodular goiter, toxic adenoma, thyroid cancer, struma ovarii, iodine excess (including radiocontrast, amiodarone)

causes of primary hyperthyroidism

TSH-secreting pituitary tumors, trophoblastic (hCG-secreting) tumors, gestational thyrotoxicosis

causes of secondary hyperthyroidism

subacute thyroiditis, silent (painless) thyroiditis, postpartum thyroiditis, excess thyroid hormone intake, drug induced (amiodarone, iodine, lithium, interferons, tyrosine kinase inhibitors, immune checkpoint inhibitors)

thyrotoxicosis without hyperthyroidism

- nervousness, fatigue, weakness, increased perspiration, heat intolerance, tremor, hyperactivity, irritability, palpitations, appetite changes (usually increased), weight change (usually weight loss), menstrual disturbances, frequent bowel movements or diarrhea - hyperactivity, tachycardia, atrial fibrillation (especially in elderly adults), hyperreflexia, warm/moist skin, ophthalmopathy or dermopathy (Graves' disease), goiter, muscle weakness

signs/symptoms of hyperthyroidism

_____ (high/low) TSH level signifies thyrotoxicosis, FT4 is ______ (high/low) in overt hyperthyroidism, almost all patients with Graves' disease will have positive TSHR-SAb and positive anti-TPOAb

low, high

ophthalmologic changes, eyelid retraction, vague eye discomfort or excess tearing, thyroid dermopathy over the lateral aspects of the shins, thyroid clubbing or acropathy

unique clinical features of Graves' disease as compared to other causes of thyrotoxicosis

many manifestations of hyperthyroidism appear to be mediated by beta adrenergic system so these drugs are used to rapidly relieve palpitations, tremors, anxiety, and heat intolerance, these can only be used until more specific antithyroid therapy is effective because these drugs do not reduce the synthesis of thyroid hormones

beta blockers

which type of beta blockers are used in hyperthyroidism? why?

nonselective (propranolol or nadolol) because they can impair the conversion of T4 to T3

large doses of iodide inhibit the synthesis and release of thyroid hormones, most commonly used in Graves' disease patients before surgery and to quickly reduce hormone release in patients with thyroid storm, frequent toxic effects are hypersensitivity reactions and iodism (palpitations, depression, weight loss, pustular skin eruptions, gynecomastia)

iodide (saturated solution of potassium iodide SSKI or Lugol's solution)

these drugs inhibit thyroid hormone synthesis by interfering with the thyroid peroxidase mediated iodination of tyrosine residues in thyroglobulin, used as primary therapy for Graves' disease or as preparative therapy before surgery or radioactive iodine administration, overall low rate of adverse effects but serious adverse effects can occur (skin rash, arthralgias, GI upset, hepatotoxicity, agranulocytosis)

PTU (can also inhibit the conversion of T4 to T3), methimazole

this drug produces thyroid ablation without surgery, iodine is concentrated in the thyroid gland, thyroid cells that have taken up iodine begin to develop abnormalities and necrosis, eventually thyroid cells are destroyed and hormone production is reduced, slow onset of action so most patients are treated with a beta blocker initially to avoid thyroid storm, may cause painful thyroiditis

radioactive iodine

subtotal thyroidectomy indicated in patients with very large goiters or thyroid malignancies or cannot tolerate other therapies/did not respond to other therapies

surgery

- S/S: high fever, tachycardia, tachypnea, dehydration, delirium, coma, GI disturbances - precipitated in a previously hyperthyroid patient by infection, trauma, surgery, radioactive iodine treatment, sudden withdrawal from antithyroid drugs - treated with short acting beta blocker like IV esmolol, IV or oral iodide, large doses of PTU or methimazole, supportive care with acetaminophen to suppress fever, fluid and electrolyte management, antiarrhythmic agents, IV hydrocortisone because of potential presence of adrenal insufficiency

thyroid storm

growth and dissemination of ___________ are stimulated by TSH so LT4 is important component of management because it suppresses TSH secretion

thyroid carcinomas

contains two iodine atoms, blocks conversion of T4 to T3, inhibits entry of T3 into cells and decreases T3 receptor binding, rapid reduction in serum T3 levels, increases free and total T4 levels, increases TSH, patients receiving this must receive monitoring (baseline serum TSH, FT4, FT3, anti-TPOAb, TSHR-SAb, should be checked 3 months after initiation and then every 3-6 months

amiodarone

associated with hypothyroidism and may occur years after therapy, inhibits thyroid hormone synthesis and secretion, may require LT4 replacement even if this drug is discontinued

lithium

causes hypothyroidism in some patients being treated for hepatitis C infection, mechanism not known

interferon alpha

hormone that helps to promote growth of the follicle in preparation for ovulation by causing granulosa cells lining the follicle to grow and produce estrogen, peak levels just prior to ovulation

follicle stimulating hormone (FSH)

hormone that promotes androgen production by theca cells in the follicle, promotes ovulation and oocyte maturation, converts granulosa cells to cells that secrete progesterone just after ovulation, peak levels just prior to ovulation

luteinizing hormone (LH)

spotting or bleeding during which week is caused by insufficient estrogen so the adjustment to be made is increased estrogen or triphasic with lower early progestin?

week 1

spotting or bleeding during which week has a difficult to determine cause so the adjustment to be made is to increase both estrogen and progestin?

week 2

spotting or bleeding during which week is caused by insufficient progestin and the adjustment that can be made is a monophasic OC with increased progestin or triphasic with increasing progestin?

week 3

patients who have been diagnosed with dyslipidemia should be switched to progestin with ______ (lower/higher) androgenicity and some examples of this are...

lower, norgestimate, norethindrone, drospirenone

a patient consistently experiences headaches during the placebo week of her OC, which formulations could you switch her to?

24 combination hormone tabs, 2 estrogen only, 2 placebos (shorter hormone free interval and may allow for shorter periods and menstrual related symptoms), monophasic combination that is 91 day treatment cycle with 84 active tabs and 7 placebos (allows for one menstrual cycle per season/4 per year)

which combined OCs are FDA approved for acne and are also considered to have low androgenicity?

norgestimate, norethindrone, drospirenone

contain a synthetic estrogen and one of several steroids with progestational activity, primary mechanism of preventing pregnancy is through inhibition of ovulation, other mechanisms include reduced penetration of the egg by the sperm, reduced implantation of fertilized eggs, thickening of cervical mucus to prevent sperm penetration into the upper genital tract, slowed tubal motility which may delay transport of sperm

combined hormonal contraceptives (CHCs)/combined oral contraceptives (OCs)

reduction in risk of endometrial cancer, reduction in risk of ovarian cancer, improved regulation of menstruation and reduction in risk of anemia, reduction in the risk of fetal neural tube defects, relief from symptoms associated with premenstrual dysphoric disorder, prevention of benign breast disease, prevention of ovarian cysts, decrease in symptoms related to endometriosis, improvement of acne control

benefits of OCs

sexually transmitted infections, cardiovascular events and hypertension, venous thromboembolism, gallbladder disease, hepatic tumors, cervical cancer, breast cancer

risks of OCs

history of thromboembolic disease, history of stroke or current cerebrovascular disease, history of or current cardiovascular disease/ischemic heart disease/peripheral vascular disease, history of carcinoma of the breast (known or suspected), history of any estrogen-dependent neoplasms (known or suspected), undiagnosed abnormal uterine/vaginal bleeding, pregnancy (known or suspected), breastfeeding less than 21 days postpartum, heavy smoking (15 or more cigarettes daily) by women who are 35 years old or older, history of hepatic tumors (benign or malignant), acute liver disease, migraine headaches with aura

absolute contraindications for combined oral contraceptive use

smoking (less than 15 cigarettes a day) at any age, migraine headaches without aura, hypertension (unacceptable when systolic over 160 or diastolic over 90), fibroid tumors of the uterus, breastfeeding greater than 21 days postpartum, superficial venous thrombosis (acute or history), multiple sclerosis with prolonged immobility, diabetes, family history of dyslipidemia, sickle cell disease, active gallbladder disease, age over 50, elective major surgery requiring immobilization

relative contraindications for combined oral contraceptive use

this type of contraceptive is preferred/recommended for women who are at increased risk of cardiovascular or thromboembolic complications because it is believed that estrogen component of CHCs stimulates enhanced hepatic production of clotting factors

progestin only contraceptives

a patient is taking a chronic medication that increases the metabolism of CHCs by induction of CYP3A4 and is being prescribed a combined oral contraceptive, what do you recommend?

recommend using an alternative non-hormonal method of contraception/backup during treatment with CYP3A4 inducer

marked by the final menstrual period resulting from loss of follicular activity and confirmed by 12 months of amenorrhea, FSH is greater than 40 IU/L and a fivefold increase in LH can be seen but the increase in LH is not required to make a diagnosis

menopause

transitional period prior to menopause when hormonal and biologic changes begin, begins with onset of menstrual cycle irregularities/other menopausal symptoms, may still ovulate intermittently during this time

perimenopause

vasomotor symptoms like hot flashes or night sweats, sleep disturbances, mood changes, genitourinary syndrome of menopause (GSM, genital symptoms like dryness/burning/irritation, urinary symptoms like dysuria/urgency/retention/recurrent urinary tract symptoms, sexual symptoms like dryness/dyspareunia), new onset depression, problems with concentration/memory

clinical presentation of menopause

when is use of a progestin required?

women who have an intact uterus should be prescribed a progestin in addition to estrogen due to increased risk of endometrial cancer/hyperplasia with estrogen monotherapy/unopposed estrogen

type of HRT administration, estrogen is administered daily, progestin is administered for 12-14 days of the month, menses returns in about 90% of women 1-2 days following the last progestin dose, women may view this scheduled bleeding as an advantage as it limits spotting

continuous estrogen and cyclic progestin

type of HRT administration, estrogen and progestin are administered daily and can result in endometrial atrophy, women do not experience withdrawal bleeding but may experience unanticipated breakthrough bleeding or spotting, this type of HRT administration offers the best protection against endometrial hyperplasia and cancer, if bleeding persists beyond 6-12 months women should seek medical attention to rule out endometrial hyperplasia or cancer

continuous combined estrogen and progestin

first line dosage form for vulvovagnial atrophy? is a progestin used with this dosage form?

topical vagianl preparations for women with moderate to severe GSM who do not respond to lubricants and moisturizers, vaginal estrogen does not require supplementation with progestin in women using low doses but women with an increased risk of endometrial cancer may warrant endometrial surveillance

which has systemic absorption - Femring or Estring?

Femring

this refers to exogenous hormones that are identical to those produced in a woman's body (estradiol, estrone, estriol, progesterone) that are either commercially manufactured or custom compounded into formulations like topical creams/gels or suppositories

bioidentical hormones

nausea, headache, bloating, breast tenderness, breakthrough uterine bleeding, coronary heart disease, stroke, venous thromboembolism, breast cancer, gallbladder disease are all adverse effects of ______ (estrogen/progestins)

estrogen

nausea, headache, weight gain, bleeding, irritability, depression, decreased bone mineral density are all adverse effects of ________ (estrogen/progestins)

progestins

- relief from vasomotor symptoms, pharmacotherapy individualized and reassessed every 6-12 months, extended treatment duration may be warranted for relief of persistent VMS and prevention of bone loss - relief from GSM, topical vaginal preparations or systemic if VMS are also present

benefits of HRT

what is the recommended duration for HRT?

4-5 years, should be tapered at discontinuation to limit the recurrence of hot flashes, slowly discontinuing HRT over 3-6 months after 4-5 years of therapy is considered reasonable and associated with less risk of recurrent symptoms while mitigating the increase in breast cancer risk that occurs at this time

type of cells that are involved with resorption or breakdown of bone and continuously create microscopic cavities in bone tissue

osteoclasts

type of cells that are involved in bone formation and continuously mineralize new bone in cavities created by other type of cells

osteoblasts

low bone mineral density, female sex, age 65 and older, race/ethnicity, history of previous low trauma/fragility fracture after age 50, osteoporotic fracture in a first degree relative, low BMI or body weight, premature menopause, secondary osteoporosis, rheumatoid arthritis, oral glucocorticoid therapy, current cigarette smoking, excessive alcohol intake, loss of height

risk factors for osteoporosis

- conditions: alcoholism, chronic kidney disease, COPD, Cushing syndrome, cystic fibrosis, diabetes, eating disorders, GI disorders, hematologic disorders (hemophilia), hyperparathyroidism, hyperthyroidism, hypogonadal states, immunologic diseases (HIV/AIDS, rheumatoid arthritis), organ transplantation, renal failure, skeletal cancer (myeloma), vitamin D deficiency - drugs: anticoagulants (heparin, warfarin), anticonvulsants (phenytoin, phenobarbital, primidone, valproic acid), aromatase inhibitors (anastrozole, exemestane, letrozole), cytotoxic agents (methotrexate, cisplatin), glucocorticoids (5 mg of prednisone equivalent for at least 3 months), gonadotropin releasing hormone analogs, immunosuppressants, lithium, medroxyprogesterone acetate, PPIs, SSRIs, SGLT2 inhibitors, thyroid supplements, TPN

causes of secondary osteoporosis or bone

many patients with osteoporosis are _______ (symptomatic/asymptomatic), when is this not true?

asymptomatic UNLESS they experience a low trauma fracture

the number of standard deviations from the mean bone mineral density (BMD) in healthy young white women

T-score

number of standard deviations from the mean bone mineral density (BMD) of age and sex matched controls, corrected for both age and sex of the patient, used more often clinically in premenopausal women, men younger than 50, patients who may have secondary causes for low BMD

Z-score

what is the recommended standardized approach to bone mineral density measurement?

central measurement of BMD by DXA scan at total hip, femoral neck, lumbar spine

women 65 and older, men 70 and older, perimenopausal women and men aged 50-69 with risk factors, anyone with a fracture after age 50, adults with secondary cause for this

recommended groups for BMD measurement for osteoporosis

what is the recommendation for calcium intake?

1000 mg for men between 51-70, 1200 mg for women older than 51 and men older than 71

what is the maximum amount of calcium that can be taken at one time? what amount of calcium can lead to toxicity?

500-600 mg at once, intakes over 1200-1500 mg/day may increase risk of developing kidney stones, supplementation over 2500 mg/day can lead to hypercalcemia, hypercalciuria, and increased risk of cardiovascular events

which patients may prefer calcium carbonate? calcium citrate?

calcium carbonate needs to be taken with food to maximize absorption, older adults or patients taking PPIs or H2 receptor antagonists may have difficulty absorbing calcium supplements due to reduced stomach acidity so calcium citrate may be a better option in these patients because it doesn't need an acidic environment for absorption and can be taken with or without food

history of hip or vertebral fracture, T score -2.5 or less at femoral neck or spine, osteopenia and at least a 3% 10 year probability of hip fracture or at least a 20% 10 year probability of major osteoporosis related fracture as determined by FRAX

patients recommended for treatment of osteoporosis

an additional tool developed by WHO to evaluate an individual's 10 year probability of developing hip and major osteoporotic fractures based on femoral neck T-score, age, and other risk factors

FRAX

- inhibit bone resorption via actions on osteoclasts or on osteoclast precursors, decreases the rate of bone resorption leading to an indirect increase in bone mineral density, decreases bone resorption by rapidly binding to the bone matrix and inhibiting osteoclast activity - take after an overnight fast with plain water while sitting upright for at least 30/60 minutes prior to morning meal, do not crush or chew - osteonecrosis of the jaw - prevention and treatment

bisphosphonates

- selective estrogen receptor modulator (SERM), selective binding activates estrogenic pathways in some tissues and antagonizes estrogenic pathways in other tissues, acts as an estrogen agonist in the bone to prevent bone loss (decreases bone resorption increasing bone mineral density and decreasing fracture incidence), overall reduces bone resorption and decreases overall bone turnover - may be taken with or without food - treatment

raloxifene

- peptide sequence similar to the human version of this, functionally antagonizes the effects of parathyroid hormone, directly inhibits osteoclastic bone resorption, inhibits bone resorption by binding to osteoclast receptors - alternate nostrils on a daily basis (nasal spray) - treatment

calcitonin

- recombinant formulation of endogenous parathyroid hormone containing amino acid sequence, similar activity as parathyroid hormone, stimulates osteoblast function increasing bone mineral density, bone mass, strength - inject into thigh or abdomen, keep pen refrigerated - treatment (men and women)

teriparatide

- analog of human parathyroid hormone related peptide which acts as agonist at PTH1 receptor, stimulation of osteoblast function and increased bone mass - inject into abdomen, keep refrigerated - treatment (PM)

abaloparatide

- monoclonal antibody that binds to RANKL and blocks the interaction between RANKL and RANK (receptor located on osteoclast surfaces), prevents osteoclast formation leading to decreased bone resorption and increased bone mass - inject into upper arm, upper thigh, or abdomen, keep refrigerated - treatment (PM and men)

denosumab

- inhibits sclerostin (regulatory factor in bone metabolism that inhibits the signaling pathway that regulates bone growth) increasing bone formation and to a lesser extent decreases bone resorption, increases production of mature osteoblasts

romosozumab

what is the maximum duration of use for Forteo and Tymlos (teriparatide and abaloparatide)?

treatment not recommended beyond 2 years due to unestablished safety and efficacy with long term treatment

presents as a recurrent headache that is severe enough to interfere with daily functioning, can be with or without aura, can be triggered by changes in behavior/environment/diet/hormone levels, these headaches occurring 15+ days per month for a 3-month period or longer classified as chronic, two or more of the following are present (pain interrupts or worsens with physical activity, unilateral pain, pulsating pain, moderate-to-severe intensity)

migraine

type of headache, pain usually reported to be mild to moderate in severity, non-pulsating, bilateral, described as band like tightness or pressure around the head, two or more of the following are present and are not aggravated by routine physical activity (bilateral pain, non-pulsating, mild or moderate intensity, no nausea/vomiting, either photophobia or phonophobia not both)

tension headaches

type of headache, severe/intermittent/short in duration type pain, typically occur at night but attacks may occur multiple times per day, described as explosive/excruciating, at least one or more of the following (lacrimation, nasal congestion/rhinorrhea, eyelid edema, forehead or facial sweating/flushing, sensation of fullness in the ear, miosis and/or ptosis (droopy eyelid), sense of restlessness or agitation

cluster headaches

highest prevalence in women 18-44 years old, more common in women throughout the age groups likely to be due to hormonal differences

migraine risk factors

more common in women, environmental factors as opposed to genetic predisposition play a central role in development of this type of headache

tension risk factors

more frequent in men, onset most common between 20-40 years, genetic predisposition is apparent though affected individuals often also present with additional risk factors like history of tobacco use, caffeine intake, alcohol abuse

cluster risk factors

defined as transient focal neurologic symptoms that can occur prior to or during a migraine, typically present as wavy lines or spots within the field of vision but can also present as scotoma (blind spot/area of reduced vision in the visual field)

aura

- behavioral: emotional let down, fatigue, sleep excess or deficit, stress, vigorous physical activity - environmental: flickering lights, high altitude, loud noises, strong smells like perfumes, tobacco smoke, weather changes - food: alcohol, caffeine intake/withdrawal, chocolate, citrus fruits, bananas, figs, raisins, avocados, dairy products, fermented pickled products, missing meals, MSG, Asian food, seasoned salt, nitrites in processed meats, saccharin/aspartame, tyramine - medications: cimetidine, estrogen or OCs, indomethacin, nifedipine, nitrates, reserpine, theophylline, withdrawal due to overuse of analgesics/benzodiazepines/decongestants/ergotamine

potential triggers of headache

why is it important to start pharmacologic abortive treatment early for acute headache?

poor drug absorption accompanying migraine attacks/enteric stasis so larger doses of oral medications may be necessary for pain relief

limit exposure to triggers, resting in dark quiet area, behavioral interventions (relaxation therapy, cognitive behavioral therapy, stress management training), alcohol in moderation, limiting tobacco use

nonpharmacologic management of headaches

when might a longer elimination half-life be beneficial when treating with a triptan?

during a long lasting migraine attack

is rimegepant (Nurtec ODT) abortive or prophylactic?

both

is ubrogepant (Ubrelvy) abortive or prophylactic?

abortive

is zavegapent (Zavzpret) abortive or prophylactic?

abortive

MOA: high affinity, highly selective 5-HT1F receptor agonist, selective targeting of this receptor is hypothesized to decrease stimulation of trigeminal system and treat migraine pain without causing vasoconstriction

lasmiditan (Reyvow)

MOA: selective agonist for serotonin (5HT1B and 5HT1D receptors) in cranial arteries, causes vasoconstriction and reduces sterile inflammation correlating with relief of migraine

triptans

what is the difference between Reyvow and triptans?

Reyvow does not cause vasoconstriction and targets a different serotonin receptor compared to triptans

which dosage forms might be helpful for treating a migraine patient who is experiencing nausea?

nasal sprays, injections

what options are available for treating an acute tension headache?

OTC analgesics like NSAIDs or acetaminophen, can use prescription strength NSAIDs or acetaminophen with an opioid analgesic if necessary

this type of headache occurs when patients use ergotamines, triptans, opioids, or other combinations for longer than 10 days per month or nonspecific analgesics for more than 15 days per month

rebound/medication overuse headache

why aren’t oral triptans the best choice for treatment of acute cluster headache treatment? what other triptan dosage forms are a better option?

delayed onset of action so injectable or intranasal triptans would be better

what is the primary novel therapy for abortive treatment of cluster headache?

administration of high flow rate oxygen

what options (besides triptans and oxygen) are available for treatment of cluster headaches?

octreotide (somatostatin analog that has short half life and may be administered SC with no vasoconstrictive effects) glucocorticoids provided IV and later tapered orally

what options are available for adjunctive therapy for migraine patients experiencing nausea?

antiemetics like metoclopramide or prochlorperazine

when is prophylactic treatment of migraines warranted?

if headaches are frequent/severe, significant disability occurs, pain-relieving medications are used frequently, adverse effects occur with acute therapies

what medications are mainstay of tension headache prophylaxis?

TCAs, muscle relaxants

which medications are mainstay of cluster headache prophylaxis?

lithium, verapamil

most triptans can be repeated after how many hours? how about naratriptan?

2 hours, naratriptan 4 hours

which CGRP is approved for cluster headaches?

emgality

benign prostatic hypertrophy (BPH) is the most common benign neoplasm in men who are at least ______ years old

tissue in the prostate that produces prostatic secretions including prostate specific antigen (PSA)

glandular tissue

tissue in the prostate that can contract around the urethra and bladder outlet when stimulated, enlarged in BPH

stromal tissue

_________ (testosterone/estrogen) stimulates glandular tissue growth but do not have a direct effect on stromal tissue

testosterone

________ (testosterone/estrogen) may stimulate stromal tissue growth

estrogen

voiding symptoms including urinary frequency, nocturia, urgency with or without incontinence

irritative

voiding symptoms including urinary hesitancy, decreased force of urinary stream, straining to void, intermittency (urinary stream that stops and starts)

obstructive

what type of factor refers to anatomic obstruction of the bladder neck caused by an enlarged prostate (as the gland grows around the urethra the prostate occludes the urethral lumen) and this factor is obstructive or irritative?

static factors, obstructive

what type of factor refers to excessive stimulation of alpha 1A adrenergic receptors in the smooth muscle of the prostate, urethra, and bladder neck which results in smooth muscle contraction and reduces the caliber of the urethral lumen, and this factor is obstructive or irritative?

dynamic factors, obstructive

what type of factor refers to bladder detrusor muscle hypertrophy in response to prolonged bladder outlet obstruction, detrusor muscle fibers undergo hypertrophy so that the bladder can generate higher pressure to overcome bladder outlet obstruction, hypertrophic ladder muscle becomes irritable contracting abnormally in response to small amounts of urine in the bladder, and this factor is obstructive or irritative?

detrusor factors, irritative

how much is drug treatment expected to decrease the AUA symptom score by?

30-50% or 3 or more points

what is appropriate treatment for a BPH patient with mild symptoms?

watchful waiting

what is appropriate treatment for a BPH patient with moderate to severe symptoms (no BPH complications), any size prostate? what about with irritative voiding symptoms? what about with erectile dysfunction?

alpha 1 adrenergic antagonist add anticholinergic or mirabegron with irritative symptoms add tadalafil with erectile dysfunction

what is the appropriate treatment for a BPH patient with moderate to severe symptoms (no BPH complications), prostate greater than 30 grams? what if they also have irritative voiding symptoms?

5 alpha reductase inhibitor OR 5 alpha reductase inhibitor + alpha 1 adrenergic antagonist if irritative voiding symptoms can add anticholinergic or mirabegron

what is appropriate treatment for a BPH patient with severe symptoms (no BPH complications)?

5 alpha reductase inhibitor + alpha 1 adrenergic antagonist

what is appropriate treatment for a BPH patient with severe symptoms and BPH complications?

surgery

mild AUA symptom score moderate AUA symptom score severe AUA symptom score

0-7 8-19 more than 20

androgens, alpha adrenergic agonists, anticholinergic agents, caffeine, anticonvulsants, diuretics, antidepressants (SSRIs), opiates, sedatives

medications that can cause/worsen BPH voiding symptoms

refers to preferential inhibition of alpha 1A receptors which comprise 70% of alpha 1 receptors in the prostatic stroma, prostatic urethra, bladder neck, these alpha adrenergic antagonists have the potential to produce less hypotension than other alpha 1 adrenergic antagonists because they have a lower likelihood of antagonizing alpha 1B adrenergic receptors in peripheral vasculature

uroselective agents - alfuzosin, tamsulosin, silodosin

which 5 alpha reductase inhibitor is selective for Type II isoenzyme and which is non-selective inhibitor of both Type I and II? are they therapeutically interchangeable?

finasteride is selective for Type II, dutasteride is non-selective, no difference in clinical efficacy, therapeutically equivalent

which BPH agents relax smooth muscle?

alpha antagonists and tadalafil

which BPH agents reduce size of enlarged prostate, reduce frequency of BPH related complications, decrease PSA, no cardiovascular effects?

5 alpha reductase inhibitors

floppy iris syndrome and orthostatic hypotension are common ADRs for which BPH agents?

alpha adrenergic antagonists

sexual dysfunction is common ADR for which BPH agents?

5 alpha reductase inhibitors

xerostomia (dry mouth) is a common ADR of which BPH agents?

anticholinergics

hearing loss, hypotension, priapism, visual disturbances are common ADRs of which BPH agents?

tadalafil

angioedema, cardiovascular effects, urinary retention are common ADRs of which BPH agent?

mirabegron

this BPH agent should be reserved for patients with both BPH and erectile dysfunction or those with LUTS (lower urinary tract symptoms) that are not responsive to alpha adrenergic antagonists, relaxation of smooth muscle of the urethra/prostate/bladder neck, relaxation of the detrusor muscle, relaxation of vascular smooth muscle

tadalafil

this BPH agent is indicated when a patient has bothersome irritative voiding symptoms despite treatment with an alpha adrenergic antagonist, typically added to alpha adrenergic antagonist

anticholinergic

beta 3 adrenergic agonist that causes release of NE which stimulates beta 3 adrenergic receptors reducing irritative voiding symptoms, not FDA approved for BPH but can be helpful as alternative therapy, typically added to an alpha adrenergic antagonist

mirabegron

these are contraindicated in people with sickle cell disease and history of priapism, should be used with caution in those taking oral anticoagulants/have bleeding disorders, generally these are more acceptable to older patients in stable relationships/infrequent sexual encounters

vacuum devices

prostaglandin E1 analog that produces an erection by stimulating adenyl cyclase leading to increased cAMP, smooth muscle relaxation, rapid arterial flow, and increased penile rigidity, available as an injection or suppository, use with caution in patients with sickle cell disease, those taking anticoagulants, bleeding disorders, increased risk of priapism and bleeding

alprostadil

these agents selectively inhibit PDE5 which is responsible for degradation of cGMP, smooth muscle is induced leading to an erection, only effective in the presence of sexual stimulation to drive the NO/cGMP system, facilitators not initiators

PDE inhibitors (tadalafil, sildenafil, vardenafil, avanafil)

when is testosterone the initial treatment of choice for ED?

in patients with low serum testosterone levels since it corrects decreased libido, fatigue, muscle loss, sleep disturbances, depressed mood

what medical conditions are contraindications to testosterone therapy?

prostate cancer, erythrocytosis, uncontrolled HF, sleep apnea

how long should patients be treated with testosterone supplementation before initiating additional ED therapy?

3 months

which types of insulin are rapid acting (bolus)?

lispro, aspart glulisine

which types of insulin are long acting (basal)?

glargine, detemir, degludec, humulin

autoimmune disease in which the insulin producing beta cells of the pancreas are destroyed leaving the individual insulin deficient

type 1 diabetes

form of autoimmune diabetes hallmarked by a milder autoimmune process and slower progression of beta cell failure as compared with type 1, adult age at onset, presence of islet autoantibodies, insulin dependence

latent autoimmune diabetes in adults (LADA)

usually slow and progressive in its development, risk factors include first degree family history, overweight/obese, habitual physical inactivity, race/ethnicity, previously identified A1c between 5.7-6.4%, HTN, low HDL or high triglycerides, history of gestational diabetes, history of cardiovascular disease

type 2 diabetes

glucose is stored here with glycogen, glycogenolysis converts stored glycogen back to glucose, glucose is primarily supplied to the brain by stores of glycogen here during fasting, during exercise most glucose is supplied through gluconeogenesis that happens here stimulated by epi and NE

liver

insulin and glucagon are produced here, beta cells produces insulin and amylin whereas alpha cells produce glucagon, main function of insulin is to decrease blood glucose and elevated BG is necessary for insulin release above basal levels

pancreas

what fasting plasma glucose results are consistent with a diagnosis of diabetes?

greater than or equal to 126 mg/dL

what postprandial plasma glucose results are consistent with diagnosis of diabetes?

greater than or equal to 200 mg/dL with symptoms of diabetes like polydipsia, polyuria, unexplained weight loss

what A1c results are consistent with a diagnosis of diabetes?

greater than or equal to 6.5%

what fasting plasma glucose results are consistent with a diagnosis of prediabetes?

100-125 mg/dL

this occurs when there is a lack of insulin peripheral tissues cannot take up and store glucose, causes body to think it is starving and ketones are produced as byproducts of free fatty acid metabolism in the liver, excessive amounts of ketones formed leads to body getting rid of them through urine leading to dehydration, patients prone to this should test for ketones during stressful events like acute illness, women with preexisting diabetes before pregnancy or with gestational diabetes should be prescribed ketone strips and educated on prevention/detection

diabetic ketoacidosis

what types of insulin are used in a pump? can either T1DM or T2Dm patients use an insulin pump?

regular or rapid acting (rapid more common), insulin pumps may be used to lower blood glucose in any type of diabetes but patients must be on multiple daily insulin injections so patients with type 1 are always candidates and type 2 are sometimes candidates

use of this device may improve blood glucose levels, reduce wide fluctuations in BG levels, and allow individuals to have more flexibility in timing and content of meals/exercise schedules for improved quality of life

insulin pumps

causes of this include delayed or inadequate amounts of food intake (especially carbs), excessive doses of sulfonylureas/insulin, exercising when insulin doses are reaching peak effect, inadequately adjusted drug therapy in patients with impaired renal or hepatic function

hypoglycemia

when is glucagon indicated and how is it administered?

patients with hypoglycemia experiencing a loss of consciousness should be given glucagon, IM or SC, patient should be rolled on side since common ADR is vomiting

what electrolytes need to be replaced in DKA? what is used for fluid replacement? what type of insulin is preferred?

potassium, normal saline for fluid replacement, regular insulin

life threatening condition similar to DKA that also arises from inadequate insulin but occurs primarily in older patients with type 2 diabetes, lacks the ketonemia and acidosis, key diagnostic criteria for this are plasma glucose levels greater than 600 mg/dL, arterial pH greater than 7.3, serum bicarbonate greater than 15 mEq/L, minimal ketonemia/ketonuria

HHS

critically ill patients should be started on what route of administration of insulin? not critically ill patients?

IV, scheduled SC

patients should monitor their BG levels more frequently on these days because it is common for this to increase BG levels, should check glucose and urine for ketones every 4 hours, should continue to take medications, should maintain normal caloric/carb intake, drink fluid to avoid dehydration

sick days

when nutrients enter the stomach and intestines, this hormone is released which stimulates insulin secretion, this effect is mediated by GLP-1 and GIP

incretin

kidneys hold onto glucose rather than letting glucose be dumped into the urine to help correct hyperglycemia, glucose filtered by the kidneys is completely reabsorbed when BG values are normal but once BG levels get higher than 180 mg/dL glucose begins to be spilled into excreted urine, this transporter reabsorbs majority of filtered glucose in proximal tubule, when these transporters are inhibited there will be an increase in excretion of glucose by the kidney which lowers glucose concentrations in the plasma

SGLT2

what is the oral drug of first choice in a type 2 diabetes patient without cardiovascular disease, HF, liver or kidney disease, or the need for weight loss?

metformin

what is first line therapy for type 2 diabetes patients with ASCVD or indicators of high CVD risk? what if they are still above A1c goal after this?

GLP-1 with proven CVD benefit or SGLT2i, then add other agent if not at goal

what is first line therapy for type 2 diabetes patients with HF?

SGLT2i

what is first line therapy for type 2 diabetes patients with CKD?

SGLT2i or GLP-1 with proven CKD benefit, if not at A1c goal add other agent

agents with efficacy for weight loss in type 2 diabetes patients

semaglutide, tirzepatide, dulaglutide, liraglutide, SGLT2i

agents with efficacy for achievement and maintenance of glycemia goals in type 2 diabetes patients

dulaglutide, semaglutide, tirazepatide, insulin, metformin, pioglitazone, SGLT2i, sulfonylurea, DPP-4i

initiation of basal insulin

start 10 units per day OR 0.1-0.2 units/kg/day

titration of basal insulin

increase by 2 units every 3 days to reach FPG goal without hypoglycemia

initiation of bolus insulin

4 units per day OR 10% of basal insulin dose

titration of bolus insulin

increase dose by 1-2 units OR 10-15% twice weekly

which agents have benefits in MASH patients?

GLP-1, dual GLP-1/GIP, pioglitazone

which agents have benefits in MACE patients?

metformin, SGLT2i, GLP-1, pioglitazone

which agents have benefit in HF patients?

SGLT2i

Final Exam :( Flashcards

(390 cards)