Unit 3: ACS, OA, PUD, IDA

S/Sx of Heart attack

chest pain that may spread to back, neck, jaw, or arms, dizziness, N/V, Rapid/irregular heartbeats, SOB, weakness

Define UA (unstable angina) and what makes it different from other ACS forms

frequent chest pain, ischemia without necrosis, no biomarkers present, no ECG abnormalities

Define NSTEMI and what makes it different from other ACS forms

form of heart attack, seen on ECG with ST segment depression or T wave inversion, troponins can be elevated by 20% or more, a non-transmural infarct in cardiac muscle

Define STEMI and what makes it different from other ACS forms

most severe form of heart attack, troponins elevated, seen on ECG with ST segment elevation, transmural infarct in cardiac muscle

Besides ST segment changes what can indicate an MI has occurred and when do we see it?

pathological q waves, 1-3 days after event

Most common cause of ACS

rupture of fibrous cap of plaques leading to thrombus forming and blocking off artery

How much of an artery is blocked in NSTEMI and STEMI

NSTEMI-partially blocked; STEMI- full blockage

Diagnostic biomarker for ACS and why is it important?

troponins, specfic to myocardial injury, fast time to peak levels, stay elevated after MI

Purpose of angiography in ACS

helps us identify blocked coronary arteries

Diagnosis criteria for ACS

2 of these: Elevated troponin plus defined by pt history, ST changes on ECG, imaging showing new regional wall motion abnormality

Role of TIMI scores in ACS

used in NSTEMI to select a management strategy

TIMI score low Risk

0-2, GRACE score <109

TIMI score intermediate risk

3-4, GRACE score 109-140

TIMI score high risk

more than 5 pts, GRACE score >140

PCI definition

a non-surgical heart procedure using stents to open blocked arteries

Acute supportive care during ACS

O2 if sat is <90%, morphine or fentanyl- analgesics for refractory chest pain, nitroglycerin- analgesic, aspirin, Beta blocker

Nitroglycerin Acute supportive care dosing

SL tab 0.3-0.4 mg q5 min for 3 or less doses

Aspirin acute supportive care dosing

162-325 mg chewed and swallowed ASAP (non-enteric coating)

How soon should Beta blocker be initiated in ACS

within 24 hrs to reduce reinfarction risk and ventricular arrhythmias

NSAIDs in ACS? (other than aspirin)

NO, CONTRAINDICATED

Selective-invasive/noninvasive Management of NSTEMI

non-invasive testing to determine if angiography needed OR treat with meds only; lower risk scores only

Routine invasive management of NSTEMI

angiography and revascularization; timing determined by risk; low- before discharge, intermediate- within 72 hrs, high- within 24 hrs

Immediate PCI STEMI management

Preferred over fibrinolytics; door to balloon time of 90 minutes

Primary fibrinolytics STEMI management

Alternative treatment- done if <12 hrs from Sx AND PCI can’t be done within 120 min, AND door to needle time < 30 min OR PT not agreeable to PCI

When is DAPT used in ACS?

ALL patients get ASA plus P2Y12 inhibitor

Aspirin loading and maintenance dose

162-325 mg; 81 mg daily

Clopidogrel loading dose and maintenance dose

600 or 300 mg once; 75 mg daily

Prasugrel loading and maintenance dose

60 mg once, 10 mg daily; 5 mg daily if <60kg or over 75 yo

Ticagrelor loading and maintenance dose

180 mg once, 90 mg BID for 12 mo then 60 mg BID if extended beyond 1 year

First line P2Y12 for ACS patients who underwent PCI

ticagrelor or prasugrel

First-line P2Y12 for non-invasive NSTEMI

ticagrelor only

Parenteral Anticoagulation in ACS: What and when

UFH only while in hospital

Parenteral anticoagulation PCI alternatives and when to stop

Enoxaparin/bivalirudin(Hx of HIT) ; stop after PCI

Parenteral anticoagulation non-PCI alternatives and when to stop

Enoxaparin/fondaparinux; stop after 2-8 days or at discharge

Which parenteral anticoagulations are IV

UFH and bivalirudin

How long is DAPT with ASA + P2Y12 continued after event?

1 year

IF DAPT risk/benefit score is what do you continue P2Y12 for more than 1 year?

greater than or equal to 2

When do we continue BB indefinitely after ACS?

if HFrEF (LVEF <40%)

What statins should a patient be initiated or increased to after ACS?

HI-statin; Atorva 40/80, Rosuva 20/40

Should ACEi or ARB be initiated or continued after ACS?

Yes, to reduce risk of all-cause death and MACE

Should aldosterone antagonist be initiated/continued after ACS?

Yes for those whose LVEF <40% and symptomatic HF or DM

Non-pharm lifestyle modifications after ACS

Improved diet- less fatty things, fruits, veggies; exercise- up to 150 min/week, will work up to that

DAPT high bleeding risk protocol

Stop ASA or P2Y12 after 1 month

Therapy that may be added to DAPT to decrease bleeding risk?

PPIs

OA treatment goals

reduce pain, increase mobility, enjoy life, reduce ADRs

Non-pharm for OA treatment

OT/PT, Exercise, weight loss, braces for knee OA, hand exercise for hand OA, tai chi

Pharmacological treatment for OA

topical NSAIDs, oral NSAIDs, topical capsaicin, APAP, Duloxetine, Suzetrigine

Which therapies are strongly recommended for hand OA?

exercise, Self efficacy/management, oral and topical NSAIDs

Which therapies are conditionally recommended for hand OA?

acetaminophen, Duloxetine

Which therapies are recommended against in hand OA (strongly in bold)

topical capsaicin, glucosamine, chondroitin

Which therapies are strongly recommended in knee OA?

exercise, weight loss, Self-efficacy/management, Tai Chi, topical and oral NSAIDs

Which therapies are conditionally recommended in knee OA?

APAP, Duloxetine, topical capsaicin

Which therapies are recommended against in knee OA?

Glucosamine, Chondroitin

Which therapies are strongly recommended in hip OA?

Oral NSAIDs, exercise, weight loss, self efficacy/management, Tai Chi

Which therapies are conditionally recommended in hip OA?

APAP, Duloxetine

Which therapies are recommended against in hip OA?

glucosamine, chondroitin

Topical capsaicin MOA

inhibits TRPV1 receptor which prevents pain action potential from occurring

ADRs of topical capsaicin

application site burning, pain, erythema, dizziness, passing out

Max dose of APAP

4 gm/day

When are NSAIDs CI in OA?

if patient has HF or CKD

Suzetrigine MOA

selective Na 1.8 channel, inhibits pain signal transmission

Suzetrigine ADRs

itching, rash, muscle spasm

primary use for suzetrigine

after joint replacement surgery

Pathophys of OA

Increase wear and tear on joint changes DNA expression, which leads to an increase in pro-inflammatory mediators which leads to cartilage breakdown and pain, increased vascularization leads to abnormal bone growth

Etiology of OA

obesity, trauma, genetics, decreased sex hormone levels (why we see in women after menopause), muscle weakness, infection

S/Sx of OA

older pts, pain, deep aching character, pain on motion, joint stiffness, instability of weight-bearing joints,

NSAIDs MOA

inhibition of COX enzymes (1 and 2) which prevents creation of pain and inflammatory mediators

Non-selective NSAIDs example

aspirin

COX-2 selective NSAIDs examples

celebrex

Semiselective NSAIDs examples (more COX 2 than 1)

meloxicam, etodolac, diclofenac

NSAIDs ADRs

GI effects, renal effects, electrolyte imbalance with salicylates, Reye’s syndrome in children, photosensitivity with profens, CNS effects with indomethacin

Which NSAIDs are more prone to GI ADRs but can provide small amounts of cardioprotection?

non-selectives

Which NSAIDs are less prone to GI ADRs but can increase CV risk

selectives

Which NSAIDs are more prone to HSRs?

non-selectives

ADME of NSAIDs

Absorbed primarily by SI, extensively plasma protein bound, hydrolyzed or glucuronidated, renal elimination

NSAID use for OA in NSTEMI

start with topicals, then APAP/dulox, then non-cox2 NSAIDS, then COX-2 NSAIDS

NSAIDs in PUD

they can induce PUD, treat PUD with PPI, H2RA or sucralfate and stop NSAID, but if can’t then reduce dose or change to celebrex, if NSAID must be continued after then combo NSAID/PPI

Pathophys of PUD

Caused by either H. pylori infection, NSAID induced, or stress induced (ischemia due to crit care condition)

Gastric PUD specific S/Sx

located in lesser curvature or atrium, Pain worse when eating, Pain better when not eating or after eating, Often asymptomatic

Duodenal PUD specific S/Sx

Upper duodenum, Pain worse 1-3 hours after eating, Pain sometimes relieved by food

General PUD S/Sx

epigastric pain, dyspepsia, GI bleeding, systemic infection, severe N/V

NSAID-Induced PUD Treatment

STOP NSAID, PPI for 8 weeks, indefinite if NSAID needs to be continued

Labs to rule out H. pylori PUD

CBC (shows bleeding), endoscopy, rapid urease test, UBT, serologic antibody, fecal antigen test

Treatment for h. pylori induced PUD

PPIs, PCABs, H2RAs, Antibiotic, Bismuth salts

Optimized Bismuth quadruple for H. pylori PUD

PPI, bismuth subcitrate or subsalicylate, Tetracycline, and Metronidazole, all for 14 days

When to test for H. pylori?

before and after treatment, test 4 weeks after treatment for cure

Rifabutin Triple therapy for H. pylori PUD

Omeprazole, Amoxicillin, Rifabutin

Follow up for H. pylori PUD after bismuth quadruple treatment?

Test for cure 4 weeks after bismuth, 2 weeks post PPI

Which tests for H. pylori PUD require holding PPIs or bismuth?

Rapid urease test and Urea breath test (2 week hold for PPI, 4 weeks for bismuth)

S/Sx of Iron-deficiency anemia

General anemia: pallor, palpitations, SOB, fatigue; IDA-specific- hair loss, pica, nail bed pitting

Dietary sources of iron

fortified cereals, clams, white beans, beef/liver, lentils, spinach, tomato, potato

Lab values present in IDA

Hgb/Hct low, MCV low, MCHC low, platelets sometimes high until iron therapy, decreased serum ferritin, low iron, increased TIBC, low transferrin saturation

Causes of IDA

blood loss, pregnancy, blood donor, elite athletes, dialysis, H. pylori, HF, celiac, Meds (PPIs/NSAIDs), other rare reasons

Treatment for IDA

oral iron supplementation; Contraindicated in celiac disease or bariatric surgery (malabsorption issues)

IDA Counseling

empty stomach increases absorption; antacids, PPIs, and H2RAs decrease absorption of iron; take 2 hours prior to PPI, H2RA, treat for 3 months (indefinite if causative factor still there maybe)