Med Surg Exam 4

What are inflammatory disorders of the heart?

Infective endocarditis Pericarditis Myocarditis Rheumatic fever

What are the common diagnostic tests used for these inflammatory disorders?

1) H/P2) 12 lead 3) Chest xray 4) Echocardiogram 5) Labs6) Blood cultures to help identify cause and direct treatment

What are the 2 most common types of echocardiograms?

Transthoracic echo: probe across chest, non invasive Transesophageal echo: probe goes through esophagus

What are the layers of the heart?


What is myocarditis, infective endocarditis, pericarditis & rheumatic fever?

Inflammation of the specific layers of the heart.Rheumatic fever can effect any & all layers of the heart

What is endocarditis?

Colonization of cardiac valve endocardium

How does endocarditis occur?

Damage to valves from turbulent blood flow leads to thrombi formation on valves > bacteria in blood attach to thrombi found in the valves > vegetations form on valves

What are septic emboli?

Vegetation from heart valves that break off and travel to other areas of the body

The vegetation on the heart valves protect themselves by forming...


Spread of endocarditis can cause...

Damage to valves and supporting structures > dysrhythmias, valve dysfunctions, heart failure, sepsis & heart block

What bacteria is the leading cause of infective endocarditis?

Gram +: Staph aureus (most common), strep & enterococci

What are the risk factors for infective endocarditis?

1) Age 2) IVDA3) Prosthetic valves 4) Dialysis

What is prosthetic valve endocarditis? When is it caused by surgery vs community acquired

Endocarditis of prosthetic valves Days to weeks after surgery = contamination from surgery 2 months after surgery = community acquired

How is infective endocarditis diagnosed?

1) Blood cultures 2) Sep set of blood cultures + for bacteria 3) Echo to show lesion (vegetation)

What are the manifestations of IE?

1) Nonspecific s/s of infection: fever, chills, etc. 2) New or worsening systolic murmur 3) Septic emboli: splinter hemorrhages and janeway lesion4) Immune reactions to septic emboli: Osler's nodes, roth sots, glomerulonephritis 5) Heart failure

Infective endocarditis may require prosthetic heart valve replacement due to damage of heart valves from infection. What are indication that this needs to be done?

1) Valve dysfunction leading to heart failure 2) To prevent embolism 3) Uncontrolled infection

How to treat infective endocarditis?

1) Blood cultures > antibiotics 2) Valve replacement (need to treat with antibiotics, not effective treatment on its own)3) Monitoring with echo and inflammatory markers

How long is antibiotic therapy for infective endocarditis?

6 weeks or more. Monitoring will continue every few months as well to make sure infection is gone by checking echo and biomarkers

How do we know if antibiotic treatment is working?

Monitor temp and WBC count. Blood cultures will also be drawn q24-48 grs to ensure clearance of bacteria from blood stream

What patient education should be given regarding infective endocarditis?

1) Avoid sick people 2) Avoid excessive fatigue/stress 3) Maintain good oral hygiene4) Consult HCP about invasive procedure for prophylatic antibiotics

Pericarditis can lead to...

Pericardial effusion > cardiac tamponade

What are the causes of pericarditis?

Infections: bacterial (tb), fungal (rare), viral (most common, coxsackievirus B) Non-infections: Dressler syndrome/post MI syndrome (4-6 weeks after STEMI)

What are the clinical manifestations of pericarditis?

P: Pulses paradoxusE: EKG changes R: RUBI: Increased JVDC: Chest pain

How would patients with pericarditis describe their chest pain?

Chest pain that is worse when laying down and when they inhale , but better when sitting up. Progressive, sharp chest pain

When auscultating what sound may you hear in a patient with pericarditis? What does it sound like and where is it best heard?

Pericardial friction rub, heard best at ERBs point. To distinguish heart from breath sounds, have patient hold breath, if it stops = pleural friction rub, if it continues = pericardial friction rub

What EKG changes help to diagnose pericarditis? How does this compare to STEMI?

Pericarditis = diffuse ST segment elevation, this will be found on all leadsSTEMI = ST elevations will only be found on certain leads, localized

What is pericardiocentesis?

Procedure that removes fluid from around the heart. Used to diagnose and help treat. Fluid can be sent to lab for cultures.

What is the presentation of cardiac tamponade?

1) Becks triad2) Tachycardia 3) SONB 4) Pulses paradoxus

What is Becks triad?

1) Low BP: narrow pulse pressure 2) Muffled heart sounds 3) JVD

What is pulses paradoxus?

Drop in SBP by more than 10mmHG during inspiration

How does cardiac tamponade impact the LV?

Fluid build up pushes on RV bowing septum into LV > less space available in LV to fill due to bowing >decreased preload, SV, CO = decreased SBP

What is the treatment of acute pericarditis?

1) Identify reason: infectious of non-infectious 2) Position: HOB at 45 3) Pain meds: ibuprofen & colchicine 4) Pericardiocentesis

What patient education should be given about colchicine?

Diarrhea is a common side effect, no grapefruit juice: decrease drug clearance

What is chronic constrictive pericarditis?

Scarring of the pericardium from acute pericarditis resulting in restriction of the heart causing a decrease in CO. Mimics heart failure

What is the treatment for constrictive pericarditis?

Pericardiectomy: removal of the pericardium to allow heart to move more freely

What patient education will be given to patient post pericardiectomy?

1) Avoid heavy lifting 2) Call HCP if: fever, increase in drainage, pain or other symptoms3) Follow post op instructions about meds, exercises, diet & wound care

What are the causes of myocarditis?

1) Idiopathic (50% of cases) 2) Viral3) non-infectious: autoimmune & cocaine ]4) Myocarditis & pericarditis

What makes myocarditis difficult to treat?

Non-specific signs 7 symptoms and is usually a mild, temporary issue

What is rheumatic fever? Rheumatic heart disease?

Rheumatic fever: An acute inflammatory disease that can involve all the heart layers Rheumatic heart disease: A chronic scarring and deformity of the heart valves resulting from

What causes rheumatic fever?

Autoimmune: Strep throat > mimics protein M > causing formation of cross reactive AB resulting in body attacking itself

What are risk factors for rheumatic fever?

1) Age 5-15 2) Gender: Rheumatic fever = same in both genders Rheumatic heart disease = more in females than males 3) Environment: High occurrence with poverty, poor access to health care, overcrowding

zHow does rheumatic fever present?

1) Itis of the heart (50% of cases)2) Mitral regurgitation 3) Joint pain: SHARP, asymmetric migrating polyarthritis 4) Skin: erythema marginatrum and SUBQ nodules 5) CNS: Sydenham's chorea

What is the most common cause of mitral stenosis?

Rheumatic heart disease

How will joint pain present with rheumatic fever?

Asymmetric migrating polyarthritis. One side and moves up body. Will have local signs and symptoms of joint inflammation

What is erythema marginatrum? Where is is commonly found?

Rash, non-itchy with prominent red border and clear center. It will intensify with heat. Found on trunk, upper and inner arms and thighs.

What are SUBQ nodules? Where are they found?

Bundles of collagen on extensor surfaces, freely moveable, hard, and painless

What is Sydenhams chorea?

Uncoordinated, involuntary jerky movements on face and all 4 limbs

How do you diagnose rheumatic fever?

Jones criteria and evidence of group A strep infection

What are the aspects of Jones criteria?

Carditis Arthritis (monoarthritis, polyarthritis, polyarthralgia) Erythema marginatum SUBQ nodules Sydenham's chorea

How do we teat for group A strep?

Rapid antigen detection test: results in 10min. If patient is within age range for rheumatic fever and RADT is negative, throat culture will be done to confirm due to high susceptibility to rheumatic fever

What is antistrepolysin-O titer?

Used to see if a patient has an antibodies for strep, not used in diagnosis as it doesn't tell us when infection was

How is rheumatic fever treated?

1) Prevention: Treat strep infection early, oral penicillin o amoxicillin for 10 days 2) Bed rest 3) NSAID for joint pain and fever

IM penicillin, what are the advantages and disadvantages?

Advantages: 1x dose (helps with compliance) Disadvantages: Very thick, painful when injected

What patient education should you give after treatment of rheumatic fever?

Need to prevent reoccurrence of rheumatic fever, you are more susceptible now, will need to take polylactic antibiotics. Teach patient tp recognize signs & symptoms of recurrence and antibiotic treatment

How long will patient be on prophylactic antibiotics?

Depends of underlying conditions. May be until age 20 or lifelong

What re nursing considerations for all the cardiac itis situations?

1) Improve CO2) Manage signs & symptoms of heart failure 3) Comfort

What is valvular stenosis?

Cant move blood forward, doesn't open properly

What is valvular regurgitation?

Cant move blood forward, doesn't close properly

Which chamber of the heart will have increased workload in stenosis and regurgitation?

If it is bi/tricuspid = atria If its pulmonic/aortic = ventricles

What are 2 common acquired causes of stenosis and regurgitation?

Rheumatic heart disease (leading of mitral stenosis), infective endocarditis

What is a congenital cause of stenosis/regurgitation?

1) Tetralogy of fallout > leads to pulmonic stenosis > RV hypertrophy 2) Pulmonic regurgitation > physiologic (incidental finding) or latergenic: S/P treatment for TOR 3) Bicuspid aortic valve: patient has structural bicuspid aortic valve

What are manifestations of stenosis and regurgitation if L heart valves are impacted? R side?

Left side heart valves: exertional dyspnea, angina, fatigue, syncope, orthopneaRight side heart valves: Peripheral edema, hepatomegaly, JVD, exertional dyspnea, angina, fatigue, syncope

All valvular disease cause and increase of decrease in CO?

Decrease > this can cause chest pain due to poor perfusion

What kind pf shock can acute mitral or atrial regurgitation cause?

Cardiogenic shock > impact CO

What are signs and symptoms of cardiogenic shock?

HypotensionTachycardiaWeak thready pulse Cool, pale. moist skin Decreased urine output Crackles, tachypnea

What is a water hammer pulse? What condition is it most commonly associated with?

A strong quick beat that collapse immediately, occurs in severe chronic aortic regurgitation

What causes a water hammer pulse?

1) Rapid systolic rise: aortic run off increase preload > increasing SV2) Diastolic collapse: most of the blood drips back into the heart (aortic run off) > decreasing CO, causing widened pulse pressure 3) Compensation for decrease in DBP > L ventricle dilates due to increased preload > myocardium to tire out, can lead to systolic failure

How can you test for a water hammer pulse?

Can find it by raising the arm and feeling the radial pulse: elevate the arm above the shoulder so that the volume of the blood can fall by gravity

What is a mid systolic murmur?

A harsh, high pitched heart sound that peaks between S1 and S2

What are other names of a mid systolic murmur?

Ejection murmur, crescendo-decrescendo murmur

A mid systolic murmur is hear when there is __________ or __________?

Pretty Ass Stones: pulmonic or aortic stenosis

What is a holosystolic murmur?

High pitched, blowing sound heard during the SI and S2 making it hard to distinguish between the two

What are other names for a holosystolic murmur?


A holosystolic murmur is heard when there is _________ or _________?

Tricuspid or mitral regurgitation

What is an early diastolic murmur?

A soft, high pitched sound heard at the beginning pf diastole and tapers off

What is another name for ab early diastolic murmur?

Decrescendo murmur

An early diastolic murmur is hear when there is ________ or ______?

Aortic regurgitation or pulmonic regurgitation

What is mid to late diastolic murmur?

A low pitched sound that starts at the beginning of diastole and disappears then begins again right before S1

A mid to late diastolic murmur is heard when there is ________ or ________?

Tricuspid or mitral stenosis *Most likely mitral as tricuspid stenosis is rare

What conditions cause systolic murmurs?

SL valve stenosis or AV valve regurgitation

What conditions cause diastolic murmurs?

SL regurgitation or AV valve stenosis

Where can each type of stenosis/ regurgitation best be heard while auscultating?


What is the focus of treatment in valvular disease? What treatment may the patient receive?

Preventing exacerbation of heart failure, acute pulmonary edema, thromboembolism and recurrent rheumatic fever and infective endocarditis

What does percutaneous transluminal balloon valvuloplasty?

Helps to open up stenosed valve

What should the nurse assess for after percutaneous transluminal balloon valvuloplasty?

Bleeding or hematoma at groin side site, infection, dysrhythmias

Is valvular repair or surgery preferred?

Repair is preferred as it has a lower mortality rate, some patients are candidates for replacement but depends on the situation

Valve repair is most often seen in which valvular diseases?

Mitral or tricuspid disease

What are the two types of prosthetic heart valves?

1) Biological: human, bovine, or porcinel, last 8-10 years, less durable due to calcification, produce more natural pattern of blood flow than mechanical valves 2) Mechanical: Made of metals, last >20 years

Which type of valve will require life long anticoagulation?

Mechanical due to increase risk of thromboembolism

Both types of valve replacement are subject to......

Leaking and risk of infective endocarditis

Why do patients with prosthetic valves need to let dr know about invasive procedures and teeth cleaning?

Increased risk of infective endocarditis, need prophylactic antibiotics

What is cardiomyopathy? What are the 3 discussed class?

A group of diseases that directly affect the myocardial structure or function. Hypertrophic, restrictive and dilated

What is the most common cardiomyopathy?

Dilated cardiomyopathy

What is occurring in dilated cardiomyopathy? What can it lead to? What heart sound may be heard with this? How will this look on echo?

LV dilated (increased compliance) > systolic heart failure. May hear an S3. Echo enlarged heart with thinned myocardium

What is occurring in hypertrophic cardiomyopathy? What does this cause? How would this look on an echo?

Septal hypertrophy of upper septum > outflow obstruction. On echo this will appear as asymmetric hypertrophy with banana shape

What is restrictive cardiomyopathy? What does this lead to? What heart sounds will you hear? What will you see on echo?

Least common. Pathological infiltrations > stiffens and firms LV making it noncompliant > diastolic heart failure. May hear S4 sound on echo will look relatively normal.

What is the most common cause of sudden cardiac death in young people?

Hypertrophic cardiomyopathy

What are causes of each type of cardiomyopathy?

Dilated: Most idiopathic or secondary to other diseases Hypertrophic: GeneticRestrictive: Amyloidosis: misfolded proteins, Sarcoidosis: granulomas, hemochromatosis, secondary to cancer radiation

What is takotsubo cardiomyopathy?

Also known as broken heart syndrome it is transient apical ballooning syndrome that is induced by stress

What does takotsubo mimic?

Acute coronary syndrome

What population is takotsubo more common in?

Postmenopausal women. If is does occur in men = worse prognosis and high risk for complications

Why does the left ventricle apex balloon in takostubo?

During a stressful event catecholamines are released causing direct myocardial toxicity and microvascular spasm/dysfunction > the catecholamines bind to adrenoreceptors on the heart (more of these are found on the apex) > the mid and the apical segments of the ventricle do not contract but the basal walls do

Why is takotsubo more common in post menopausal women?

Decrease om estrogen that has cardioprotective effects > post menopausal women have exaggerated VC and SNS activation in response to psychosocial stress

How might the patient with takotsubo present? Mimicks ACS

Chest pain DyspneaPalpitations SyncopeECG changes Mild elevation of trops

What are the ECG changes with takotsubo?

Diffuse (found on several different leads) ST elevation and diffuse DEEP symmetric T wave inversion

Will a patient with takotsubo have an abnormal angiogram?

NO at most will show mild to moderate coronary atherosclerosis (<50% occlusion)

How to diagnose takotsubo?

1) ECG: Diffuse ST elevation and deep T wave inversion and troponin (mild elevation only)2) Echo: hypokinesis =, akinesis or dyskinesis (paradoxical movement) of the L ventricle apical and or mild segments 3) Cath lab: Absence of obstructive coronary disease or less than 50%

What is the treatment of takotsubo?

Treatment similar to ACS and give supportive management (MONA BASH)

When does systolic function return in patients with takotsubo?

Within 2 months, it is a self limiting condition

What is physiological splitting?

Occurs due to breathing causing delayed closure of pulmonic valve giving a split S2 sound

What is the function of the esophagus? What type of tissue does it contain, what can damage this tissue?

Move food from mouth to stomach. Made of stratified squamous epithelium > does not have defense mechanism like the stomach epithelium making it susceptible to acid damage

What are the different secretory cells of the gastric pit in the stomach?

G cells, chief cells, parietal cells, mucus cells

What is the function of the G cells?

Release gastrin in response to food > gastrin release stimulates parietal cells

What is the function of parietal cells?

Release HCL (food breakdown and kill bacteria) and intrinsic factor: absorption of B12 > problems with this can cause pernicious anemia

What is the function of chief cells?

Release pepsinogen > pepsinogen and HCL > pepsin to break down proteins

What is the function of mucus cells?

Produce mucus > bicard to help neutralize the acidity

What is the role of prostaglandins in the GI tract?

1) promote mucus and bicard production 2) VD: increase BF to gastric mucosa > can increase risk of bleeding

Drugs used for GI: Acid reducers vs neutralizers

H2 blockers:OTC, end in -tidine, famotidine & cimetidine PPIs: end in -prazole OTC, omeprazole & lansoprazole & esomeprazole Rx pantoprazole & dexlansoprazole & rabeprazole Antacids: Aluminum hydroxide & calcium carbonate & magnesium hydroxide & sodium bicarbonate

What is the difference between H2 blockers and PPIs?

H2 blockers: block histamine binding to H2 receptors of parietal cells, have a quicker onset than PPIs and shorter duration PPIs: block the proton pump, preventing the release of H+, MOST potent acid reducer, slower in onset than H2, but longer duration

What is a commonly given mucosal protectant?

Sucralfate: PO tablets or oral suspension

H1 blockers are non-selective and work both CNS and peripherally what does this mean?

Can have many CNS effects > sedation due to crossing BBB, can block cholinergic, a adrenergic, and serotonin receptors

What are indications for H2 blockers?

1) short term use for GERD, gastric/duodenal ulcers, hypersecretions, etc. 2) Prophylactic stress ulcer in hospital setting

What are nursing considerations for H2 blockers?

Used for gastric symptom relief or prophylactically 30-60 mins before known food or beverage triggers Once daily dosing: give at bedtime Twice daily dosing: give 30-60 mins before breakfast and dinner Pts should not initially self treat for longer than 2 weeks without consulting with PCP

What education should you provide to patients about the use of OTC PPIs?

1) Not intended for immediate heartburn relief (takes 1-4 days for full effect 2) Should only be used for 14 day, up to 3 times a year

What are the adverse effects of PPIs? What does this mean for patients?

Many adverse effects. Infections: decrease acid content > can't kill bacteria, vitamin deficiency, increased risk of fractures, decrease risk. Should give lowest doses for shortest amount of time possible

How should PPIs be given?

Need to be given before eating! 1x dosing > give 30-60mins before breakfast 2x dosing > give 30-60mins before breakfast & 30-60 mins before dinner

If PPIs & H2 inhibitors are both prescribed how should they be taken?

H2 blocker can decrease PPI effects > need to take PPI in morning and H2 blocker at bedtime

What are some common antacids? What is their MOA?

Aluminum hydroxide Calcium carbonate Magnesium hydroxide Sodium bicarb They help to neutralize HCl acid Antacids produce quick, short-lived relief of heartburn

What in the benefit to antacid combination products?

They can counteract the adverse effects and make them more tolerable to take

What are the adverse effects of antacids?

Aluminum hydroxide & calcium carbonate > constipation Magnesium hydroxide > diarrhea Sodium bicarb > metabolic alkalosis

What are the nursing consideration for antacids?

1) Quick, short lived relief for heart burn 2) Most effective after meals and at bedtime 3) give with 8oz of water 4) Combo products help prevent constipation and diarrhea 5) Give 1-2 hours after other meds as they can decrease absorption of other meds

What are indications for sucralfate? How should it be given?

Prescription ONLY for short term treatment of duodenal ulcer treatment in PUD > provides mucosal protection. Take on an empty stomach 1-2 hours before or after food/medsWorks best with given at bedtime

What is GERD?

Common GI problems in which stomach acid flows into esophagus

GERD can cause...

1) Esophagitis 2) Esophageal stenosis 3) Abnormal cell lining > barrett's esophagus (metaplasia: premalignant condition) > adenocarcinoma

What are risk factors for GERD?

Many risk factors > factors weaken the LES and/or irritate the esophageal mucosa: 1) Obesity2) Fatty diet3) spicy foods 4) nicotine 5) Alcohol (hard & beers), carbonated drinks: bubbles expand increasing pressure on LES and acid 6) Caffeine 7) Chocolate: Acidic and weakens LES due to serotonin release 8) Peppermint and spearmint 9) Milk & dairy: Increases gastric acid release

What drugs increase risk for GERD?

1) NSAIDs2) Asthma meds: relaxes LES3) IV glucagon: relaxes LES

What are the manifestations of GERD?

1) Pyrosis: burning feeling in stomach2) Dyspepsia: pain in upper to mid abdomen3) Regurgitation > can erode teeth enamel 4) Resp symptoms: Wheezing, coughing, dyspnea 5) Otolaryngologic symptoms: hoarseness, sore throat, dysphagia, odynophagis (painful swallowing)**All of these symptoms are worse when laying down

When will GERD be the worst?

At night as symptoms are worst when laying down >> may have sleep issues

How is GERD diagnosed?

1) History and physical 2) 24hr pH impedance 3) Barium swallow 4) EGD: Upper GI endoscopy > non-dyslastic barrets (less likely to get cancer) and dysplasic

What is 1st line medical therapy for GERD?

Lifestyle modifications and PPI

Nursing considerations for EGD (esophagogastroduodenoscopy)?

Pre EGD: NPO 8hrs before Post EGD: check airways > decreased gag reflex, let them wake up then give water

What is the treatment of GERD?

1st line: Lifestyle changes (weight loss, avoid restrictive clothing, small frequent meals to avoid distention, no alcohol or smoking, decrease mint, chocolate, and spicy/fried foods

What education should be given to a patient about sleeping after eating?

Try not to sleep after eating > elevate the HOB, try to stay upright 3 hours after eating, avoid eating for 3 hours before bedtime, lay on R side to help with emptying stomach

When are drugs indicated in GERD treatment?

When lifestyle modifications are not effective

What drugs are 1st line treatment for GERD? Adjuncts?

1st line: PPIs and H2 blockers Adjuncts: Antacids

What is PUD? Where are the ulcers found?

Having one or more sores in the stomach or duodenum

What kind of environment is required for ulcer development?

An acidic environment

Do you need an excess of acid?

No there is an imbalance between gastric mucosal protective and destructive factors

What are risk factors for PUD?

1) H pylori (gram -) 2) NSAIDs 3) Cancer, chemo, radiation, viral infection, alcohol

How does PUD occur?

Risk factor > erosion > histamine release (vasodilation and increased cap permeability) > pulmonary edema and destruction of mucosal cells (decreases bicarb activity) both histamine release and destruction leads to acid and pepsin release > further damage > ulceration

What ulcers are more prevalent in women and in those over 50 yrs old?


What ulcers are more common?


Where are gastric ulcers found in the stomach?

Any part but are found commonly in the lesser curvature

Why is mortality higher for gastric ulcers?

Due to higher incidence in older populations

Why do gastric ulcers cause obstruction?

Mucosal edema from histamine release causes stomach to swell, preventing emptying

What age range do duodenal ulcers tend to occur in?


Where are duodenal ulcers typically found?

Right after pyloric sphincter

Hypertrophy of what gland in common with duodenal ulcers? Why?

Brunners gland. Hypertrophy occurs due to increase in mucous protection to help protect small intestines

Which ulcers tend to be cancerous?


How do we get h pylori?

Found naturally within human stomach, fecal to mouth, mouth to mouth

What are the virulence factors of h. pylori?

1) Flagella 2) Lipopolysaccharides 3) Urease (creates ammonia) 4) Secretes exotoxins ( VacA apoptosis and CagA: inflammation)

What issues does h pylori cause?

1) PUD2) Gastritis 3) gastric carcinoma4) MALT lymphoma

CagA & VacA can be used to help diagnose...

CagA: PUDVacA: gastric carcinoma

How to diagnose h pylori infection?

1) EGD and biopsy (gold standard) 2) Urea breath test (measurement of chemically tagged CO2 > shows active infection)3) Serology: IgG, IgA, VacA and CagA (does not tell us about active infections 4) Fecal antigen test

What diagnostic tests are used to assess if infection id eradicated?

Urea breath test and fecal antigen test: used after antibiotics to assess treatment

Why do NSAIDs cause PUD?

1) Decrease good prostaglandins > losing protection 2) if h pylori is present increases risk 3) use in conjunction with anticoagulants or corticosteroids

What is stress related mucosal disease?

physiological stress ulcers due to acute illness, burns, head injuries

Why are PPIs prescribed prophylactically?

To help prevent stress related mucosal disease

What are manifestations of PUD? Are these differences between gastric and duodenal ulcers?

Signs & symptoms of both: bloating, N/V, early feelings of fullness, burning epigastric painGastric: pain is worse with eating (physical food touching ulcers and increase of HCL in stomach, weightloss)Duodenal: No pain when eating, but 2-5 hours later, wakes them up at night

What are the 3 complications of PUD? Which are emergencies?

1) Hemorrhage2) Perforation3) Gastric outlet **All 3 are emergencies

What is the most common complication of PUD?


What are signs and symptoms of hemorrhage in PUD?

Blood in vomit/stool, diarrhea

How do we treat hemorrhage?

Give blood or fluids > Hgb level: hgb <7 given blood, surgery, embolization

What is the most lethal complication of PUD?


What is the treatment of perforation in PUD?

NG tube: decompression and remove stuff that could cause contamination, IV fluids, meds, surgery

What are sigsn and symptoms of perforation?

1) Sudden and sever abdominal pain: starts @ epigastric region then diffuse across abdomen. Rigid abdomen. Absent bowel sounds. Rebound tenderness > guarding 2) Septic shock, fever 3) Shoulder pain due to free air irritating phrenic nerve

What patient is at risk for with perforation?

Septic shock

What is septic shock?

Low BP due to exaggerated inflammatory response > too much vasodilation

What are the signs and symptoms of septic shock?

Hypotension TachycardiaFull bonding pulsesWarm, flushedFever

What is gastric outlet obstruction?

Blockage of stomach outlet due to inflammation and edema, scarring, less common issue

What are the signs and symptoms of gastric outlet obstruction?

Vomiting: Projectile with food particles, bloating, nausea, abdominal pain, loss of appetite, burning helps to feel better, pain is worse at the end of the day > may see visible swelling of the upper abdomen

How to treat gastric outlet obstruction?

NG tube: decompression > then need to address underlying cause, endoscopy: use balloon to help open up stomach and biopsy, surgery

If you have an NG tube in place should there be intermittent or continuous suction?


How to diagnose PUD?

Ensoscopy: can directly view gastric and duodenal mucosa > biopsy to assess for h pylori

How can we assess if ulcers are healing?


How do we treat PUD?

Depends on the cause: rest, drug therapy, smoking cessation, diet modifications, long term follow up care

How long does it take ulcers to go away?

Long time, months

What diet mods should PUD patients avoid?

Pepper, carbonated beverages, broth, caffeine, alcohol, dairy & spicy foods

Do diet and stress cause ulcers?

No just irritate ulcers

What drugs should PUD patients avoid? What if they need to take these?

NSAIDs and aspirin for 4-6 weeks, for those that must take these use PPI with low dose aspirin of use enteric coated aspirin

If h pylori is the reason for PUD, how is the patient treated?

Antibiotics > treat infection and PPIs for 14 days > helps to decrease acid and decrease ulceration

What antibiotics are used for treatment of h pylori?


What is flagyl?

Metrondiazole > used for gut and groin anaerobic bacteria

Sucralfate is best for treatment of which kind of ulcers?