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...
Biofilms
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?
Pansystolic
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?
Gastric
What ulcers are more common?
Duodenal
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?
35-45yo
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?
Gastric
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?
Hemorrhage
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?
Perforation
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?
Intermittent
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?
Endoscopy
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?
Duodenal