Exam 4 Flashcards
Most common cause of cardiovascular disease
Definitions:
Abnormal accumulation of fatty substances and fibrous tissues in the blood vessel walls
This reduces blood flow to the heart muscle
-Heart works heart to get blood through narrow artery and BP goes up
Fatty lipids deposited in the arterial wall –> inflammatory response –> injury to the endothelium
Atherosclerosis
Non modifiable: -Age --Men >45 years old --Women >55 years old -Gender -Race --African Americans, Mexican Americans, Native -Americans, Asian Americans -Family history: even in healthy so major prevention Modifiable -Diabetes -Hypertension -Smoking -Obesity -Physical inactivity -High blood cholesterol New risk factors: -Peridontal disease, influenza, sleep apnea (OSA: hypoxia --> heart disease; causes HTN --> artherscelorsis), increased BMI (increased abdominal girth increases risk of atherosclerosis) For a diagnosis of metabolic syndrome: need 3 or more -Insulin resistance -Abdominal obesity -Dyslipidemia -Hypertension -Proinflammatory state (HIGH LEVELS OF CRP) -Prothrombotic state (HIGH FIBRINOGEN) So DMT2
risk factors for atherosclerosis
Ischemia-inadequate blood supply that deprives the heart muscle of oxygen
Angina-chest pain due to ischemia
Myocardial infarction-if the decrease in blood supply is enough or for a long enough duration –> death of myocardial cells
Myocardial damage decreased cardiac output!!
Could lead to heart failure and sudden cardiac death due to lethal cardiac rhythm disturbances r/t increase workload on heart –> disturbed electrical pathways
manifestations of atheroscelorsis
Chest pain
Shortness of breath (especially in elderly)
Extreme fatigue
Diaphoresis
Nausea and vomiting
Women are atypical: shoulder/arm pain, jaw/back pain
How do you know the difference between angina and MI? = Angina isn’t consistent pain and goes away with meds and rest; MI is persistent pain
classic signs of myocardial ischemia
Controlling cholesterol
- High cholesterol=CAD
- Four elements of fat metabolism
- -Total cholesterol
- -LDL - bad: want them to go to liver to be excreted
- -HDL - good: makes LDL go to liver
- -Triglycerides
- -*these all affect the development of heart disease
20 yrs and older: fasting lipid panels every 5 years
under 20 with family history: tests frequently
management of CAD
Goal= low LDL and high HDL
LDL
<160 for patients with one or no risk factors
<70 for patients at very high risk for acute coronary event
How do we control these LDL levels? = Exercise
cholesterol
Treatment:
Meds that lower lipids
Monitor closely, can affect liver labs
Lifestyle changes
Dietary
Physical activity
Smoking cessation- reduce 50% in first year and continues to go down
Stress management
Hypertension management
Diabetes management
hyperlipidemia
HMG-CoA Reductase Inhibitors (STATINS) FYI -Lovastatin -Pravastatin -Simvastatin -Fluvastatin -Atorvastatin -Rosvastatin Nicotinic Acid -Niacin Fibric Acids -Fenofibrate
Bile Acid Sequestrants
- Cholestyramine (Questran)
- Colesevelam (WelChol)
- Colestipol HCL (Colestid)
cholesterol medications
Hypertension:
- Risk of CAD increases with HTN
- Increases workload of left ventricle –> stressed left ventricle –> failing
Diabetes: -Dyslipidemia -Increased platelet aggregation -Altered red blood cell function What do all of these lead to? = thrombus/clot which increases risk of CAD
hypertension and DM
Pain or pressure in the anterior chest
Caused by insufficient blood flow (usually a blocked artery)
-Oxygen demand exceeds the supply
Types of angina:
-Stable: occurs with exhortation and relieved with rest - happens with activity
-Unstable: lasts longer, more severe, can occur with rest
-Intractable/refractory: severe, incapacitating
-Variant/Prinzmetal’s: chest pain, pain at rest, ST elevation with EKF so take to cath lab and will have clean vessels/no blockage: this is vasospasm r/t ST elevation
-Silent: ischemia on EKG but no pain
angina pectoris
Mild indigestion to a heavy sensation in upper chest - From discomfort to agonizing pain Feeling of impending doom/death Radiate to neck, jaw, shoulders and arms (especially left side**) Tightness** Diabetics: neuropathy so can't feel Women: atypical S/S Weakness Numbness Shortness of breath Pallor Diaphoresis Anxiety Dizziness Nausea and vomiting
Nitroglycerin and rest make it go away
Angina S/S
12 lead EKG
Blood biomarkers: usually drawn q 8 hrs 3 times and look for peak
-CK/CKMB, Myoglobin, Troponin T* or Troponin I* (shouldn’t have any; if + it’s released in response to ___Tegrity* and leads to ischemia)
Stress test: treadmill or meds to increases HR
Nuclear scan
Cardiac catheterization: visualization (pt has chest pain, do card cath in femoral/radial artery, thread cath and visualize arteries/vessels for blockages; use dye, so worry about kidney function r/t contrast dye)
Angina diagnosis
Goal is to increase oxygen supply and decrease oxygen demand to myocardium
Oxygen 1st
Meds: beta blockers (lower HR/BP), blood thinners (esp. with concern of thrombus), Morphine (lower workload (preload) on heart), Nitro (vasodilators)
Control risk factors
PTCA AKA balloon/angioplasty/angiogram
Medical management of angina
M-morphine
O-oxygen
N-nitro
A-aspirin
PTCA or stent placement
Goal is to restore oxygen to the heart and prevent further damage
Time is muscle: door to balloon time = 60 minutes; most amount of time to restore blood/O2 supply; goal is to restore muscle
percutaneous coronary intervention
Could be emergent
Balloon tipped catheter opens vessel and resolves ischemia
Sheath inserted in either the femoral artery or radial artery through the aorta –> into coronary arteries
Balloon is inflated and deflated to open vessel
percutaneous transluminal coronary angioplasty
To prevent restenosis
Metal mesh that provides support to a vessel
What are these patients at risk for after stent placement? = clots: put them on Plavix/aspirin
pt. comes in for bleed, see hx of CAD on chart, ask if they have hx of stent, aspirin could cause the bleed
coronary artery stent
Bleeding or hematoma -Strict bedrest -Manual pressure for 30 mins -Monitor CBC-may need transfusion - shows bleeding -Hematoma: BUN/creatinine = low, tachycardia, hypotension; cough/vomit can cause this Lost or weak pulse distal to site -Assess CSM, color, compare pulses* priority Pseudoaneurysm -Notify physician -Anticipate ultrasound -Assess CSM Retroperitoneal bleed -S/S: back pain, hypotension, stop infusion and fill tank back up -Notify physician -Stop anticoagulants -Anticipate giving IVF or PRBC Acute renal failure -Hydration* with IV to flush dye out -Monitor urine output -Monitor BUN/Creatinine -Administer Mucomyst (protects kidneys so give with CAD)
complications after PTCA
Allergic reaction -Administer Prednisone, antihistamines, H2 blockers prior to the procedure if known allergy to contract or shellfish Cardiac tamponade -Anticipate pericardiocentesis Chest pain r/t stent disturbances -Notify physician -Monitor VS Chest pain (always treat; it's an emergency) -Notify physician -Monitor VS -Cardiac & pulmonary assessment -Assess EKG -Assess troponin
complications after PTCA 2
Many go home the next day Monitor for bleeding Angio seal: collagen plug to seal artery Direct manual pressure Femostop: belt across waist, inflate ball to provide pressure Bedrest Leg straight Radial site
post PCI care
PCI = PTCA and Stent
Over 65 million adults in the US Undermanaged 30% of people don’t know they have hypertension Primary hypertension -95% -Unidentifiable cause, don't know it Secondary hypertension -5% -Identifiable cause: pregnancy, renal/kidney failure (renal arter stenosis causes HTN), meds (steroids and vasoconstrictors)
hypertension
White-coat hypertension: Hypertension in the clinic - no aggressive treatment; more common
Masked hypertension: Normal BP in clinic but hypertension at home or work
-When this is suspected, what should the nurse do? = tell pt. to self home monitor; stop smoking/drinking/stress
Increased workload of heart –> Over time will lead to heart disease and stroke
hypertension types
Normotension: -Blood pressure <120/80 -Must look at this on a continuum -Assessment is based on the average of at least 2 readings --longer BP and higher it gets on trend --> increased risk of morbidity and mortality Prehypertension -Blood pressure 120-139/80-89 -Lifestyle changes: exercise, no smoke/drink, eat healthy - time to catch and fix it Hypertension stage 1: -Blood pressure 140-159/90-99 -Lifestyle changes and medication Hypertension stage 2: -Blood pressure 160 or higher/100 or higher -Medications are a must - lifestyle changes are a plus
types of hypertension
Multifactoral
Age (44) and Elderly (noncompliant; kidney/liver have decreased function, so start low and increase slow)
More common in younger men than women until menopause
Obesity - Childhood
Often coexists with dyslipidemia, diabetes mellitus, sedentary lifestyle and metabolic syndrome (increase risk of CVD with all)
African Americans-especially males
Oral contraceptive use-when accompanied with smoking & obesity
Increased sympathetic nervous system activity
Increased absorption of sodium, chloride, and water (heart failure and increased extracellular fluid –> overwork heart –> big/boggy heart –> fails
Increased extracellular fluid volume, increased systemic vascular resistance
risk factors of HTN
Heart disease
Stroke
Chronic kidney disease (low BUN/creatinine) (with HTN have nocturia)
Peripheral artery disease
Retinopathy: retina vascular damage caused by HTN
HTN damages inner lining blood vessels –> vascular damage to organs –> S/S
underlying systemic effects of heart failure
Weight reduction
DASH diet-dietary approaches to stop hypertension
-Eating plan: consistent amount of potassium, low sodium, high protein, fruit/veggie, low bad fat
Sodium restriction
Physical activity 30 mins at least 3X/week
Moderate alcohol consumption (1-2/day for men; 1/day for women)
Smoking cessation
Complimentary and alternative therapies (stress reduction: yoga, acupuncture, herbal meds but watch med interactions and do lots of teaching)
Self management: self monitor/manage at home, self diet/exercise, good teaching from nurse
nursing management of HTN
Must support patient in adherence/compliance! do everything you can to do so Most patients need 2 drugs Thiazide diuretics -Hydrochlorothiazide (K wasting), Furosemide (K wasting), spironolactone (K sparing) Beta Blockers -Atenolol, Metoprolol, Propranolol Alpha2-Agonists -Clonidine: longer acting Vasodilators: dilate blood vessels to lower BP - Hydralazine, Nitropursside, Nitroglycerin ACE inhibitors -Captropril, Enalapril, Lisinopril ARB -Losartan, Valsartan CA channel blockers -Diltazem, Amlodipine
Can reduce when BP is <140/90 for at least 1 year, so self monitor at home and bring log to apts.
*Give simplest treatment possible
Don’t stop taking r/t rebound HTN
pharm therapy for HTN
Blood pressure >180/>120
Poorly controlled HTN or stopped taking meds
More common in men, older adults, African Americans
Head injury, pheochromocytoma, food-drug interactions, eclampsia, substance abuse, renal disease
2 categories
Hypertensive urgency
-Blood pressure is severely elevated but there is no evidence of organ damage*
-Elevated blood pressure with severe headaches, epistaxis, anxiety
-*Goal-reduce bp to 160/110 for several hours to several days
Hypertensive emergency
- Blood pressure >180/120 and must be lowered quickly to stop organ damage
- Hypertension of pregnancy
- MI
- Dissecting aortic aneurysm
- Intracranial hemorrhage
- Can’t lower too quickly r/t pass out r/t decreased perfusion
hypertensive crisis
Blood vessel grafted to occluded coronary artery
Indications:
Alleviation of angina that can’t be controlled
Left main coronary artery stenosis, multi vessel CAD
Prevention & treatment of MI, arrhythmias, heart failure (blocks coronary artery and decreases blood and O2 –> tissue death; the increases work load stresses the heart)
Treatment of complications from unsuccessful PCI
coronary artery bypass graft (CABG)
open heart surgery
General anesthesia
Cardiopulmonary bypass machine (some on pump, some off pump)
Blood vessel from somewhere else (saphenous vein, left internal mammary artery-LIMA) is grafted-bypasses the obstruction
Chest tubes - anytime with open heart; drains stuff from surgery; 2-3 tubes
Pacer wires: in heart, externally stick out of skin; if brady/tachy you can hook up to this connection
MIDCAB: minimally invasive CABG with no chest incision
CABG
MI: common intra/post op from CABG; inta can decrease perfusion so it can decrease O2 to area in heart
-Know post op if they had an MI during surgery by doing EKG
Renal failure: decrease perfusion to kidneys - check I/O, output, labs BUN/Creatinine to check for decrease perfusion
Hypovolemia: most common cause of decreased CO after CABG
-Know if they have it if their tachy/hypotensive and give fluids/blood to fill tank back up
Bleeding: can cause platelet dysfunction; have low hematocrit/hemoglobin, low BP, blood in chest tube r/t internal bleed - do good chest tube assessments and monitor pleura bag
Cardiac tamponade: emergency; fluid around pericardiac sac - not a problem if you have a chest tube
Fluid overload
Hypothermia: keep warm postop to prevent vasoconstriction; cold will constrict vessel
Hypertension: with vasoconstriction; worry about pressure on heart and can rupture/bleed - give antihypertensives
Tachyarrhythmias: a fib on 3rd day r/t volume changes in body (fluid imbalances)
Bradycardias: pace monitor
Heart failure: increased work load on heart
CABG complications
Neurological status-LOC, pupils: decreased perfusion during surgery (stroke r/t clots and hyperperfusion)
- hard post op to assess r/t pain meds so know baseline*
Cardiac-heart rate, rhythm, sounds: higher HR the more decreased in CO; a fib is common; hypervolemia will have S3 sound
Pulmonary-Lung sounds, O2 saturations, respiratory rate, rhythm: note work of breathing; ex: pneumonia r/t alveoli collapse - hear crackles and know why it happened and fix the why
Peripheral vascular status-pulses, color, skin temp, edema: take vessel and bypass so check blood flow, pulse and perfusion
Renal-urine output, labs to see decrease perfusion
Fluid & electrolyte-I/O, skin turgor
Pain-assessment: *know baseline and pts. goal - do frequent vitals and control. In pain, they can’t wait/deep breath/incentive spirometer
Assess lines, tubes: chest tube, IV, pacer wires - hard to ambulate because of this - must be done
nursing care assessment for CABG
Restoring cardiac output: hypovolemia is most common cause, so give fluids/blood-give back what they lost
- watch output, labs, VS, check for a fib (r/t blood pooling) and arrhythmias
- watch mental status change to check perfusion to brain
Maintaining adequate tissue perfusion: ambulate early, watch CSM, peripheral vascular, DVT/clots*
Monitor signs/symptoms of infection: take temp, labs, watch incision site
Fluid and electrolyte imbalance: I/O, labs
Hourly blood sugar for 1st 4 hours. If >150-180 start insulin drip to bring glucose down. Glucose control is very important for healing*
Impaired gas exchange: cough/deep breath/IS 10X/hour, give O2, on vent for 1st hour, pain control, assess lungs
Impaired cerebral circulation: monitor neuro status*
Pain: can’t have good gas exchange if they don’t have good pain control
nursing interventions for CABG
Reduced blood flow
Unstable angina-plaque ruptures, artery not completely occluded
Acute coronary syndrome
Vasospasm: with prinsometals/variant angina r/t vasospam; see ST elevation
Decreased oxygen supply from blood loss (r/t decrease perfusion/tissue death) or hypotension (not enough O2 in body)
Increased oxygen demand from tachycardia, drugs (cocaine)
IMBALANCE BETWEEN OXYGEN SUPPLY AND DEMAND!
Myocardial infarction (MI)
Types:
STEMI: 100% occlusion
NSTEMI: partial occlusion
Q wave: can show MI
Chest pain- can be persistent/sudden or sometimes silent!
**EKG-T wave inverted, ST segment elevation, Q wave
Echocardiogram: ultra sound of heart to look at heart function; if MI see abnormal LV wall function
-r/t lack of O2 –> cell death –> abnormal wall movement
Labs: 1. Triponin (draw 3x/8 hours-look for peak and find downhill slide), 2. CKMB, 3. Myoglobin
manifestations of MI
Chest pain Shortness of breath, pulmonary edema Nausea and vomiting Decreased urine output Cool, clammy, diaphoretic skin, pale Anxiety, restlessness *Fear *Denial
clinical manifestations of MI
Get to the hospital! give good education, like don't drive EKG Labs *Oxygen r/t chest pain and no O2 Nitroglycerin to dilate vessels Aspirin in case of clot Beta blocker decrease BP/work of heart Ace/ARB to decrease BP
medical treatment of MI
Evaluate need to PCI: do you need cath lab? determine this off labs/EKG if theres ST elevation Thrombolytics Morphine to decrease work of heart IV Heparin, Enoxaparin - anticoag Clopidigrel - antiplatelet Bedrest to decrease work on heart
medical management of MI
Education about risk reduction
3 phases-starts with diagnosis of atherosclerosis and continues for months!
Look at page 421, box 14-7 for health promotion education-KNOW THIS!!
cardiac rehabilitation
Relieve pain PCI Aspirin, Nitroglycerin, Beta blockers Anticoagulants Morphine Oxygen *Reduce anxiety Close monitoring MONA
Monitor and report changes in the cardiac rhythm and rate closely Heart sounds* Lung sounds * Blood pressure* Pain* Respiratory status*
nursing management of MI
Function of the Kidney
- Filature out waste
- Regulates BP by fluid balance
- RBC production
- Electrolyte imbalances r/t fluid balance
Sudden
Can happen in hours to days
Oliguria = <400 mL/day (20 mL/hr)
anuria = no U.O. 50 mL/day
Increased serum BUN/CR = waste in the blood
Acidosis: S/S: blow off = resp system compensates and have increased RR and uremic smell
Fluid excess- lungs 1st AMB dyspnea/crackles, then in tissues (edema/periorbital/JVD)
Electrolyte imbalance: potassium is biggest concern - will increase w/o kidney
BP irregularities: FVE hypertension and RAS system (kidney and blood have renin and active by vasoconstriction and can’t rid waste and holds onto fluid)
Anemia: RBC regulation in kidney - w/o kidney = low hemoglobin/hematocrit
acute renal failure
Exact patho isn’t always known
Different categories
Prerenal: perfusion problem/blood flow to area; determined by MAP (average pressure blood pumps with each cycle - measures perfusion and needs to be >65)
Intrarenal
Postrenal
acute renal failure patho
Caused by any condition in which there is Decreased blood flow (MAP <65) Decreased cardiac output -MI - heart is compromised -Shock - heart is compromised -Heart failure - heart is compromised Hypovolemia: not enough fluid that can't support pressure -Dehydration -Hemorrhage -GI disturbances: colitis or diarrhea -Sepsis: drops BP
prerenal of ARF
Persistent hypoperfusion (low perfusion) –> decreased adaptation –> increases sympathetic response –> arteriole constriction –> decreases GFR –> acute renal failure (ARF)
If addressed early, no actual nephron damage/recovery can be rapid
Prolonged prerenal AR –> leads to intrarenal ARF increased mortality
prerenal of ARF
Direct insult on renal tissue
Causes
-Acute tubular necrosis (ATN) * (90% of intrarenal cases)
–Nephrotoxic agents
–Medications: contrast dye (hard on vessels of kidneys), antibiotics r/t filtered in kidneys (vancomyocin)
–Rhabodmyolysis: muscle wasting - proteins released from break down and go to kidneys and they can’t filter
–Severe transfusion reactions
–Prolonged prerenal ARF
Infections
–Crush injuries: r/t rhabodmyolysis and break down of muscles and proteins released
intrarenal of ARF
Obstruction in the urinary tract below the kidneys causes waste to build up in the kidneys (occurs after it leaves filtration system)
Hydronephrosis –> GFR decreases
Causes
- Obstruction-BPH (benign prostetic hypertrophy - blocks urethra) or kidney stones
- Obstructed foley catheter kinked
postrenal of ARF
Prerenal: give fluids r/t low volume - support pressure with meds (vasosuppressors)
intrarenal: stop giving med if that’s the cause, change abx if that’s the cause - allow kidney to rest
Postrenal: break up the stones with shock waves, put in stent to hold area open, nephrotube, ilioconduct - remove prostate if that’s the issue
interventions of ARF
fix issue/cause
Initiation
Oliguric
Diuretic
Recovery
phases of acute renal failure
Renal insult to cell injury
Can last hours to days
-MVA: physical injury can start it
BP: no BP can start it
Manifestations
- GFR decreased
- Decreasing UOP
- Alterations in fluid volume
- -Imbalance in I&O*
- -Increased weight
initiation phase of ARF
<400ml UOP/24 hrs. (20 mL/hr)
Lasts 1-2 weeks
Manifestations
- Electrolyte imbalance: low phosp, low calcium, high K, high Na, high BUN/CR, FVE, azotenia = build up of waste products
- Increased BUN/CR
- Fluid volume imbalance
NEED TO SUPPORT THE KIDNEYS! Help do their job - watch electrolytes/give meds, change diet, fluid restrict
May need dialysis
Longer in this phase –> worse prognosis (want out of phase as fast as possible)
oliguric phase
main acute injury phase
Recovery of function and continues/lasts 7-14 days
Gradual increase in urine output
Manifestations
- *Polyuria-nephrons still not fully functional-excretes waste but not able to concentrate urine - frequent/larger amount urine (more dilute/lighter)
- Gradual decrease in BUN/CR r/t removal of waste
Monitor for hypovolemia rebound: restrict so much they don’t have enough
diuretic phase
when urine output starts to increase the glomerular filtration has start to recover
Improvement of renal function
Can take up to 12 months
normal function but continue to watch kidney
recovery phase of ARF
Lethargy/ fatigue - esp with dialysis Decreased urine output -Oliguria (<400ml/day) -Anuria (<50ml/day) Nausea/Vomiting r/t GI upset/anorexia Hyperventilation r/t acidosis/trying to block off CO2 --> fast smelly respirations Diagnostic tests -Increased BUN/CR -Increased Phos/decreased -Ca++ (treat phos 1st) -Anemia: look at blood test -Hyperkalemia: dangerous; EKG changes, muscle cramps/weakness, diarrhea -EKG-peaked T waves r/t hyperkalemia -Metabolic acidosis
S/S acute renal failure
Identify and correct cause Maintain perfusion to kidneys Clear obstructions: catheter? stone? Treat shock/infection: antibiotic Diuretics: give with FVE IV fluids: to maintain fluid balance, BP and perfusion to kidneys Dialysis
management of ARF
Assessment
-Respiratory
-Cardiovascular
Frequent I/O to check what phase pt. is in
Daily weight
Fluid restriction: give hard candy to stimulate secretions, ice chips, measure liquid for them - can get FVE, damage to kidneys/heart/electrolyte imbalance
Teaching: importance and readmission
Turn, cough, deep breathe to prevent fluid in lungs/edema
Prevent infection
-CAUTI
nursing management of ARF
Monitor labs
Hyperkalemia
-Kayexalate: binds to K and rids through feces: gives pt. diarrhea - rids K and Ph
-Insulin, dextrose, calcium (short term treatment): dump insulin and pushes K back into cells - BS doesn’t like this so give with sugar
-Albuterol nebulizer
Acidosis
-Treat with Sodium bicarbonate (acts as a buffer)
May need to adjust dosage of drugs that are excreted via kidney
Meds: think what’s excreted/filtered in kidneys and adjust done PRN
management - medications for ARF
Dietary considerations
- High calorie
- Protein restriction: no banana, citrus, tomato
- High carbs
- Restrict foods high in potassium
Older adult: increased risk of rental failure r/t sensitive CR levels, decrease body mass and increase risk of dehydration
management of ARF
Chronic renal failure
-End stage renal disease (ESRD)
Irreversible
Dialysis
Risk factors
-DM r/t increase sugar in vessels –> damage
-HTN: damaged vessel and arterosceloric plaque
DM and HTN common together and have increase risk of renal failure with both
-Family history
-Elderly
Chronic renal failure/end stage renal disease (ESRD)
last stage of chronic renal failure is ESRD
Neurologic: effects brain with electrolyte imbalance: confusion, decreased LOC, lethargy, fatigue
Cardiovascular: most serious- 90% pts who die of
- heart failure, FVE, pulmonary edema, pericarditis
ESRD have heart issue
GI: diarrhea, N/V, anorexia
Dermatologic: uremic acid skin/breath
Hematologic: anemia
s/s of chronic renal failure
Creatinine: goes up 1st - more sensitive GFR (see pg. 751) Sodium: as you get fluid volume excess it can dilute out - restrict sodium TEGRITY Acidosis: low pH Anemia Calcium/Phosphorus
labs for Chronic renal failure
Phosphate binders
-PhosLo
-Os-Cal
Anti-hypertensive meds: diuretic won’t hurt kidneys - don’t give ACEs
Diuretics
Epogen-especially with dialysis: hormone used to grow RBC production and vamps up in bone marrow
Diet-
-low protein
fluid restriction-500-800ml + previous day’s 24hr urine output
-low K+, Na, Phosphorus
-Dietician consult
Dialysis
management of chronic renal failure
Education - go home on fluid restriction so educate on consequences/readmission
- Fluid restriction
- Diet
- Daily weight: same time/scale/clothes
- Treatments
- Complications: watch for edema 1st, low U.O./differences, heart palpitations, muscle cramps/weakness, dizzy, lethargy, hyperkalemia
- When to call the MD
- Follow up
Lab studies -BUN/Cr -GFR -Urinalysis Kidney ultrasound/CT scan: use dye which damages kidneys Urine output Kidney biopsy
NM of chronic renal failure
Chronic renal failure or acute renal failure Types -Hemodialysis -Peritoneal dialysis -Continuous renal replacement therapy (CRRT) Why dialysis? -Hyperkalemia -Fluid overload -Acidosis -Encephalopathy -Toxins
dialysis
Functions as the kidney
Blood –> machine –> toxins removed –> blood back to patient
1. Dialyzer-semipermeable membrane (functions as ‘kidney’)
2. Dialysate-solution made of electrolytes; adjustable based on patient need (similar to electrolytes in blood)
Anticoagulant used-keeps circuit from clotting - give heparin (check PTT 25-35 seconds)
2 large bore needles used
Osmosis-water moves from an area of higher solute concentration to lower solute concentration. *How excess water is removed
Diffusion-particles move from an area of higher concentration in the blood to lower concentration *how toxins are removed
Ultrafiltration-water moves under high pressure to lower pressure *helps water removal
hemodialysis
Temporary: higher risk of infection - for acute, not chronic
-Double lumen
-Central line
–Internal jugular
–Femoral
–Subclavian
AV fistula- best
-Assess for bruie with bell and feel thrill (vibrates) - these tell you how well it’s working
-atherscleosis, PAD, diabetics with bad vessels are poor canidates
AV graft: replace every 3 years
dialysis access
Assessment of fistula or graft
- Bruit
- Thrill
- Observe for s/s of infection (low fever, pain, drainage, red, warm)
- Drainage
No BP’s on affected arm: can change pressure/ blow vessel
No IV sticks on affected arm - tons of backflow and don’t want to risk infection/infuse anything else in there
nursing management for dialysis
Continuous vitals during dialysis to check for rebound BP/dehydration
Medication adjustment: give the meds it will take them all out - wait until after to take meds
–hard with BP meds given before therapy b/c pt. will become hypotensive with dialysis alone
Give Education and Support
dialysis management
*Hypotension Muscle cramping Dislodging of lines Dysrhythmias r/t K disturbances Air embolism Chest pain r/t electrolyte shift Dialysis disequilibrium r/t electrolyte shift Clotting - main reason fistula fails -Heparin induced thrombocytopenia
complications of hemodialysis
In the ICU setting
Continuous dialysis very slowly b/c pt is so hemodynamically unstable
For hemodynamically unstable patients
can adjust meds to compensate
continuous renal replacement therapy (CRRT)
Patients who refuse hemodialysis, don't have vessel or want freedom Patient who have no other access Patients who can’t tolerate hemodialysis Tenckhoff catheter Peritoneal membrane-dialyzing membrane Continuous or ’exchanges’ solution of med predetermined by doctor
Complication
- Peritonitis*: inflamed entire abdominal section and won’t be able to do dialysis there anymore
- Leakage around site
- Bleeding
- Incomplete emptying of fluid and need to reposition patient
peritoneal dialysis
Inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients “POOR PUMP”
heart failure
Ejection fraction (EF)- amount of blood ejected with each contraction. Normal 55-65%
Systolic heart failure-most common. Alteration in ventricular contraction by weakened heart muscle
Diastolic heart failure-stiff heart muscle. Ventricle can’t FILL properly
EF is normal in diastolic heart failure
EF is reduced in systolic heart failure
heart failure information
Pulmonary congestion
Left ventricle can’t pump blood effectively pulmonary venous blood volume & pressures increase forces fluid from capillaries into tissues and alveoli impaired gas exchange
S/S: Pulmonary congestion, Dyspnea, Cough, Crackles, Decreased oxygen saturation, Anxiety
left sided heart failure
Many times caused by left sided heart failure
Right ventricle pump failure peripheral congestion
Right side of the heart can’t eject blood and can’t handle all the blood that normally returns from venous circulation backs up into systemic circulation
S/S: Hepatomegaly, Ascites, Edema, Weight gain, Anorexia, nausea, JVD
Right side cath: Preload pressures, Pulmonary pressures, Determines severity of heart failure
Right sided heart failure
”Volume”
Volume in the left ventricle at the end of diastole
Excess preload stress on ventricular wall increased workload on heart
preload
“Pressure”
Pressure required to open the aortic valve
Increase in afterload increased stress on ventricular wall increased workload on heart
Afterload
Hearts ability to effectively contract
Can’t directly measure contractility
Sympathetic nervous system response to increase contractility
Decreased contractility increase in preload
contractility
Systolic heart failure results in decreased blood ejected from the ventricle which will stimulate the sympathetic nervous system
Heart rate will increase-(sign of worsening heart failure)
Cardiac output will decrease
Vasoconstriction of the skin, GI tract and kidneys
heart rate
How the heart compensates for the increased workload
Increased thickness of the heart muscle
Abnormal
ventricular hypertrophy
Diagnostics: Chest X-Ray, 12 lead EKG (Determines arrhythmias, if patient had MI or if theres LV hypertrophy), Echocardiogram (looks for cardiac abnormalities, measures EF), Labs, Right sided heart catheterization
Chest x-ray: Determines if the heart is enlarged and/or if there’s pulmonary congestion
-Cardiomegaly-systolic dysfunction
Labs: CBS, electrolytes, BUN/CR, liver function tests, urinarlysis, BNP
Tests for heart failure
Assessment - Manifestations of fluid overload
Health history - SOB, Orthopnea?, Edema?, ADLs?, Mental status?, Intake and output, Daily weights
Nursing care for heart failure
Ultrafiltration-similar to dialysis except this only pulls off fluid
Biventricular pacemaker-leads in right atrium, right ventricle and left ventricular cardiac vein
Implantable cardiac defibrillator (ICD)-for patients at high risk of life threatening arrhythmias
Ventricular assist device (VAD)- mechanical pump that replaces the function of the left or right ventricle
Heart transplant-replaced with a donor heart
heart failure treatments
Gastritis-inflammation of the gastric or stomach mucosa
- Acute-several hours to a few days
- Hallmark: acute onset
- Chronic-repeated exposure to irritating agents or recurring episodes of acute gastritis
Causes of acute:
-Dietary*
-Medications
-ETOH – alcohol (irritant in stomach that can damage mucosal lining and pancreatic cells)
-Bile reflux – like aspirin
-Radiation therapy
Concern about skin integrity with ulceration - if it continues it can cause bleeding
Mucous membrane-edematous and superficial erosion takes place secretes a small amount of gastric juice and a lot of mucus superficial ulceration or irritation hemorrhage
Acute gastritis
Symtpoms:
-Rapid onset: Body lets you know right away
-Abdominal discomfort
-Headache
-Fatigue
-Nausea
-Anorexia
-Vomiting
-Lack of appetite
-hiccups
Diagnosis
-Upper GI series: if serious, drink barium that coats stomach and can see where it’s narrow or inflammed
-Endoscopy: upper – long camera placed into stomach and can directly visualize what’s going on
–This is better because we can directly see it, do biopsy’s, sample it, if bleeding and clip it, and can treat while you’re in there
-Biopsy
gastritis
Self repair
Instruct patient to refrain from ETOH and food until symptoms resolve
-Watch for dehydration and correct electrolyte imbalance
May need IVF
Neutralize acid
-Antacids to neutralize acid in stomach
If severe you will have a lot of erosion-must stop vomiting due to danger of perforation
-If perforation happens, life threatening emergency (hole/bleeding/acid in abdominal cavity)
-If vomit so much worry about perforation so stick NG down them and give antiemetics
NG tube
Analgesics
Sedatives
Fiber optic endoscopy: flexible tube
Surgery if progresses to perforation or something like that: to remove gangrenous or perforated tissue, gastric resection-to treat pyloric obstruction (a narrowing of the pyloric orifice) that can’t be relieved by medical management
management of gastritis
Hiatal hernia-opening in the diaphragm through which the esophagus passes becomes enlarged and part of the upper stomach moves up into the lower portion of the thorax
Types:
-Sliding-upper stomach and the gastroesophageal junction are displaced upward and slide in and out of the thorax (accounts for 90% of hiatal hernias)
–As you eat/swallow/do things it pops up and down
–S/S: 50% are asymptomatic, often implicated in reflux
-Paraesophageal hernia-all or part of the stomach pushes through the diaphragm beside the esophagus
–Out pouch through stomach but other spot is intact
–No reflux r/t no backflow of acid – just a piece that’s pouch
–Complain of full/tight feeling when they eat r/t pressure it puts (like chest pain)
–Mimics acute coronary symptom
–S/S: sense of fullness after eating, chest pain, could be asymptomatic, reflux usually doesn’t occur, concern with obstruction r/t to cut off blood flow –> ischemia –> death/necrosis –> abscess
–hemorrhage, obstruction and strangulation can occur with all types of hernias
hiatal hernia
Hiatal hernia-opening in the diaphragm through which the esophagus passes becomes enlarged and part of the upper stomach moves up into the lower portion of the thorax
Types:
-Sliding-upper stomach and the gastroesophageal junction are displaced upward and slide in and out of the thorax (accounts for 90% of hiatal hernias)
–As you eat/swallow/do things it pops up and down
–S/S: 50% are asymptomatic, often implicated in reflux
-Paraesophageal hernia-all or part of the stomach pushes through the diaphragm beside the esophagus
–Out pouch through stomach but other spot is intact
–No reflux r/t no backflow of acid – just a piece that’s pouch
–Complain of full/tight feeling when they eat r/t pressure it puts (like chest pain)
–Mimics acute coronary symptom
–S/S: sense of fullness after eating, chest pain, could be asymptomatic, reflux usually doesn’t occur, concern with obstruction r/t to cut off blood flow –> ischemia –> death/necrosis –> abscess
–hemorrhage, obstruction and strangulation can occur with all types of hernias
hiatal hernia
Sliding
-Frequent, small meals to prevent stretching pouch
-Do not lay down for 1 hour after eating r/t turning up acid – want to keep food in stomach
–Gravity is our friend
-Elevate head of bed 4-8 inches (semi fowler to prevent heart burn while laying)
-Surgery-with esophageal injury
–S/S: 50% are asymptomatic, often implicated in reflux
Paraesophageal
-Similar to treatment of reflux
-Lower acidity, small meals, lower head of bed
-Emergency surgery
–Correct torsion (twisting) of the stomach
–Twist can lead to ischemia which can lead to necrosis
S/S: S/S: sense of fullness after eating, chest pain, could be asymptomatic, reflux usually doesn’t occur, concern with obstruction r/t to cut off blood flow –> ischemia –> death/necrosis –> abscess
–hemorrhage, obstruction and strangulation can occur with all types of hernias
Diagnose: Xray, barium swallow, fluoroscopy
Management of hiatal hernia
Gastroesophageal reflux disease (GERD)-back-flow of gastric or duodenal contents into the esophagus
(chronic amount of heartburn after you eat)
Causes
- Some of this is normal! Like in pregnacy
- Incompetent lower esophageal sphincter
- Pyloric stenosis in lower part
- Motility disorder – chronic backflow of acid to esophagus
S/S
- Burning sensation in esophagus
- Dyspepsia (indigestion)
- Regurgitation
- Dysphagia
- Hypersalivation – increase amount of secretions/gastric juices body responds by making more saliva
- Esophagitis
- *What process do these symptoms mimic? MI OR ACUTE CORONARY SYMPTOMS
gastroesophageal reflux disease (GERD)
Diagnosis:
-Endoscopy for definitive answer
-**Patient symptoms with course of proton pump inhibitors (PPI) to differentiate GERD from other disease processes
–Doesn’t clear up right away r/t decrease amount of acid made in system and must take regularly to lower acid you secrete
–GERD-usually responds to PPIs
Management:
-Teaching!
-Low fat diet and no spicy foods
-Avoid caffeine, smoking, alcohol, milk, carbonated beverages
-Don’t eat or drink 2 hours before bed r/t stimulation of juices to start working and if you lay down it will backflow to esophagus
-Maintain normal body weight
-Avoid tight fitting clothes
-*Elevate head of bed 6-8 inches: sleep on many pillows
-Sleep on pillows
-Meds = antacids, H2 receptor antagonists (Pepcid, axid, zantac) and PPI (azoles)
-Surgery: Nissen fundoplication-wrapping of a portion of the gastric fundus around the sphincter area of the esophagus
GERD
-Inflammation of the biliary system* and carcinoma
-Gallbladder inflammation-cholecystitis (inflammation of biliary system)
-Gallstones-cholelithiasis (gallstones obstruction biliary system)
–Stones plug up and attack
-Gallstones-most common disorder of the biliary system
–high fatty diets increase risk of this
–Stones are insoluble to water so can’t move anywhere
-50% of stones made up of cholesterol-insoluble in water
Diagnosis
-Abdominal US or CT scan
Gallbladder disease
On the right side
Risks:
-Obesity r/t diet changes and high cholesterol
-Females-especially with multiple pregnancies and increase age
-Frequent changes in weight
-Estrogen therapy
-Gastric bypass
-TPN
-Cystic fibrosis
-Diabetes
-Family history
S/S:
-Silent or mild symptoms that can occur after you eat
-Could be symptoms from gallbladder disease or from obstruction of bile
-Epigastric distress
-Pain
-Abscess, necrosis and perforation with continued obstruction*
-Biliary colic (gallbladder attack)- Excruciating right abdominal pain; Can come or go – usually on right side; Radiation to back or right; shoulder; Nausea and vomiting; Chills; Belching; Bloating
How do nurses know if an abscess occurs? What symptoms will they have?
Know abscess if irritation at site, erythema/warmth, tachycardia, fever, pain
With heart burn, food relieves it - with this, food worsens it
cholelithiasis
Acute inflammation of the gallbladder
-Empyema-gallbladder fills with pus
-Anything filled with pus
Calculous cholecystitis-gallbladder stone obstructs bile outflow
-Gallbladder becomes inflamed and distended
Acalculous cholecystitis-gallbladder inflammation without obstruction by gallstones
-Occurs after major surgery, trauma (tissue responds with inflammation), burns
-Could be caused by imbalance in fluid and electrolyte
Cholecystitis
S/S:
-Pain and rigidity of upper right abdomen
-Radiates to back or right shoulder or scapula
-Nausea and vomiting
-Elevated WBC
-Positive Murphy’s sign
management
- Bowel rest – don’t eat r/t that will stimulate bowels
-Management of fluid and electrolyte imbalances
-Pain management
-Antibiotics
Surgery-cholecystectomy
See page 714, box 25-11 for patient education on lap cholecystectomy
-Open gallbladder surgery – split down side and remove it
-Laparoscopic cholecystectomy – 3-5 pokes to remove it
Nursing management:
- Can go home the next day, dress or steri-strips or combo
- Tell patient to leave them alone, don’t wash or redress (they will fall off themselves), wait 24-48 hours to shower
- Activity: move right away and do IS
- Tell patient to call doctor with S/S of infection since it takes a few days to develop (fever, redness, drainage, swollen, tender) or acute pain or severe N/V
- NV is #1 complications, so start on ice chips and toast
Cholecystitis
Gastric, duodenal or esophageal ulcer
-Dull, nagging pain the worse the ulcer gets
Hollowed out area that forms in the mucosal wall of the stomach, in the pylorus, in the duodenum or in the esophagus
Stress Ulcer -related mucosal disease (stress ulcers)-acute mucosal ulceration of the duodenal or gastric area that occurs after physiologically stressful events (like mechanically ventilation, MVA)
- Clinically different than peptic ulcers
- Could be from hypovolemia/hypoperfusion r/t loss of blood to tissue and responds by erosion
Concern: bleeding – 2 types of GI bleeds, and perforation
- Slow leak: doesn’t fill up stomach, so poop out dark/tarry/coffee ground stool
- Big leak: vomit large amounts of blood
- OR perforation: ulcer bleeds into cavity and acid floods abdomen
Peptic ulcer disease
Risks
-40-60 years old
-Infection with gram negative bacteria H. pylori- doesn’t cause ulcers in everyone!
-H. pylori can contribute to excessive secretion of HCL in the stomach
-Milk, caffeinated beverages, smoking and ETOH increase HCL secretion
-NSAIDS
-Stress
-Spicy foods
-Hereditary
S/S:
-Intermittent usually – not consistent pain
-Can be silent
-Dull, gnawing pain (Sharp pain means perforation)
-Burning sensation in midepigastrium or back
-Heart burn
-Vomiting-can be from obstruction of pyloric orifice
-Bleeding (check to see by stools, H/H)
Diagnosis
-Physical exam-pain, epigastric tenderness or abdominal distention
-Barium study – swallow dye and look where erosions are
-*Endoscopy – can look and fix it while in there (can clip, staple, burn or inject with epinephrine to vasoconstrict and clot bleed)
Peptic ulcer diseaes
management
- Antibiotics to treat the H. pyloric
- Proton Pump Inhibitors (PPI) – reduce acid
- Histamine-2 (H2) receptor antagonists
- *Encourage patient to continue medications even when symptom free!
- Lifestyle changes: Stress reduction, Stop smoking, Dietary - Eat 3 regular meals, No need to eat small, frequent meals as long as antacid or histamine blocker is taken
- Surgery
- -Necessary for patients with intractable ulcers, life threatening hemorrhage, perforation or obstruction
- Vagotomy with or without pyloroplasty-transecting the nerves that stimulate acid secretion and opening the pylorus
- -Removing/clipping the vagal nerve since that’s causing the pain
- Antrectomy-removal of the pyloric (antrum) portion of the stomach with anastomosis to either the duodenum or jejunum
- -Remove bottom part of stomach since that’s where lots of ulcers form
peptic ulcer disease
Complications
- Hemorrhage or upper GI bleed-most common complication
- -Large hemorrhage-most of the blood is vomited
- -Small hemorrhage-much is passed in stool
- If a large amount of blood is vomited, what should the nurse worry about?
- What does the nurse assess? Interventions? I/O, hypovolemic, kidney function
- Perforation (hold in stomach) and penetration (leaking of acid into pancreas or other organs)
- Perforation-erosion of the ulcer into the peritoneal cavity
- This requires immediate surgery! Why?
- Penetration-erosion of the ulcer through the gastric serosa into adjacent structures such as the pancreas, biliary tract or omentum
- Symptoms of penetration-back/epigastric pain not relieved with medications
- Requires surgical intervention
- Postoperatively from surgery = NG tube and drainage/bleeding, Monitor fluid and electrolytes, Assess for s/s of infection/peritonitis
- Pyloric obstruction (gastric outlet obstruction)-area distal to pyloric sphincter becomes scarred and stenosed from spasm or edema or from scar tissue
- Patients will have nausea, vomiting, constipation, epigastric fullness, anorexia
- -If constipated with fever = infection so don’t get them something that will speed up GI tract and look for cause of infection
Treatment
- NG
- Upper GI study/endoscopy
- Balloon dilation of pylorus
- Antrectomy-if obstruction unrelieved by medical management
- Stent placement
Complicaions of peptic ulcer disease
Inflammation/edema of the appendix
-Most frequent intraabdominal emergency surgery
-Kink or occlusion
-Fecalith (harden stool)
-Tumor
-Foreign body
-Adhesions (long fibrous strip in abdomen that pinch off blood flow)
Risks
-Young (10-30)
-Winter months
-Family history
-Male
-Cystic fibrosis
Kink or occlusion –> increase in intraluminal pressure –> inflamed appendix fills with pus –> right lower quadrant pain
Diagnosis
-CBC for WBC to see infection
-Imaging = Abdominal xray, Ultrasound, CT scan
-Diagnostic laparoscopy: we think it’s this but open up to confirm
Appendicitis
Initial Onset:
-Vague epigastric or periumbilical pain
-Low grade fever
-Nausea and vomiting
-Loss of appetite
May progress to
-Right lower quadrant pain*
-McBurney’s Point/Rosvig’s Sign (press on left side and feel pain on right)
-Rebound tenderness
-Constipation or diarrhea
-Pain on urination
-Rigidity of the right recuts muscles
-Diffuse pain and abdominal distention (with rupture) (rupture can lead to sepsis which can lead to shock)
management
- Immediate surgery to prevent burst, abscess and death
-Can have S/S for a week
-Correct/prevent fluid and electrolyte imbalances
-Antibiotics
-Opioids (#1 treatment for pain like this)
-May be discharged with normal temperature and tolerable pain postop
Management of gastritis if rupture
-Abscess may form and leaks puss then organs have this on them so you need antibiotics and drain
-Antibiotics
-Drain (watch to see if it’s resolving, getting worse or getting secondary abscess)
-NG for bowel rest and to relieve nausea
-Risk for peritonitis, intestinal obstruction (treat with NG and then bowel resection), secondary abscesses
NG for suspected paralytic ileus prior to surgery
Appendicitis
Inflammation of the peritoneum
Also called “hot belly” or “acute abdomen” (distended, swelling, tight, guarding, warm, S/S of infection – fever, tachycardia, more diffused pain)
Life threatening emergency r/t entire cavity infected and effects all other organs
-May lead to sepsis, organ failure, subsequent infection
Serous membrane lining of abdominal cavity and covering the viscera
Abdominal organs leak into the abdominal cavity -> bacterial proliferation -> edema of tissues -> exudation (shift) of fluid -> hypermotility of the intestinal tract -> paralytic ileus (piece no longer moving and obstructs) -> accumulation of air/fluid in the bowel (distention)
What would cause abdominal organs to leak?? – infection and abscess – one organ has some sort of infection
Necrosis from ulcer could perforate stomach, obstruction or trauma or stab wound can lead to issue in peritoneum
Peritonitis
Risks -Bacterial infection -Disease of GI tract -Internal reproductive organs -Injury/trauma -Infection of nearby organ outside peritoneum -Abdominal surgeries -Peritoneal dialysis S/S -Diffuse pain ->constant and localized pain near the site of inflammation -Tenderness -Distention -Muscle rigidity -Rebound tenderness -N/V -Fever (100-101) -Increased HR -Elevated white count -May have low H&H r/t hemorrhage with abscess burst -Abnormal electrolytes r/t fluid shift Diagnosis Based on symptoms and labs Abdominal xrays -Free air and fluid -Distended bowel loops CT scan -Abscess formation -Inflammation/infection of organs -Perforation (concern r/t burst and fluid going to peritoneal cavity) Peritoneal aspiration: will help you test specific bacteria and treat it Management Fluid replacement (isotonic) Analgesics Antiemetics NG Monitor breathing to see shock (acidosis will compromise breathing so check stats and EKG) if it progresses and shock gets worse then you ventilate Oxygenation -> ventilation Antibiotics Surgery:Postop complications ICU care often needed Drain- watch output Arterial line I&Os and watch BP to check for damage to kidneys Fluid and electrolyte balance Position for comfort – fetal position Watch for tissue break down, keep patient comfortable,
Peritonitis
Inflammation of the pancreas – release of enzyme and pancreas starts eating itself
Acute vs chronic
Acute
-Medical emergency r/t leakage of digestive enzymes into system
-Mild will still have damage and will take up to 6 months
-High risk for life-threatening complications and mortality
Chronic
-So much pancreas has been destroyed/calcified that it’s not very functional
-May go undetected until large amount of tissue damage
-Acute does not necessarily lead to chronic
-Characterized by acute attacks
Pancreas makes insulin, release glucagon, and makes enzymes that break up fats/enzymes/carbohydrates to get nutrients
Pancreatitis
Self-digestion (trypsin) ->vasodilation, inflammation, vascular permeability ->necrosis, erosion -> hemorrhage, organ failure Risks Alcohol Drugs Gallstones will block pancreatic duct and cause issues Trauma Infections close to pancreas Autoimmune disease Duedenitis Peptic ulcer disease Ischemic vascular disease Hyperlipidemia Hypercalcemia Medications Hereditary Idiopathic (15% of cases) Mild: Inflammation and edema localized to pancreas Return to normal function in 6 months At risk for hypovolemic shock, F&E imbalances*, and sepsis Severe: Enzymes from the pancreas damage blood vessels Bleeding/ Thrombosis Necrotic tissue Pancreatic cysts/abscesses Organ failure Shock Renal failure GI bleeding
acute pancreatitis
S/S: Severe midepigastrium pain Abdominal distention May find palpable mass N/V Grey-Turner sign (result from hemorrhage around flank), Cullen sign (indicates hemorrhage around umbilicus) Mental confusion Agitation Fever Jaundice Hypotension Tachycardia Cyanosis, respiratory distress Col, clammy skin Peritonitis Guarding Diagnosis: Patient history Physical exam Labwork -Serum amylase and lipase will be sky high ** -WBCs -Hypocalcemia: the lower the calcium, the worst the pancreatitis CT scan Management: -Relieve S/S with opiods, IV fluids then TPN, strict NPO, NG to suck out everything NM: Pain relief Breathing – IS and bedrest (problems like pneumonia/atelectasis with no activity so IS is v important) -No moving r/t increase in metabolic rate which kicks in pancreas Nutrition Skin integrity r/t lack of nutrition which slows healing Monitor for complications, especially BS *
Acute pancreatitis
Progressive anatomic and functional destruction of the pancreas
Fibrous tissue replaces normal tissue after acute attacks – gets hard/calcified
Typically due to long term alcohol consumption (toxic effect on pancreatic cells)
Less common:
-Genetic mutations
-Autoimmune
-Duct obstruction
-Idiopathic
S/S:
Reoccurring acute attacks
Worsening pain, opioid dependence with each
Significant weight loss or won’t eat r/t pain
Malabsorption (decrease in lipase production)
-Steatorrhea: gut stops absorbing nutrients – gray, greasy foul smelling stool
Diagnosis:
Clinical findings and history
Endoscopic retrograde cholangiopancreatography (ERCP) – take long flexable camera down throat to look at pancreas – can use to diagnose and remove stones
MRI, CT, ultrasound
Lab analysis of steatorrhea
Management
Zero alcohol
PPIs – reduce acid
Pain management
Pancreaticojejunostomy (Roux-en-Y)
Pancreatic stenting if gallstone is main cause
Whipple resection (pancreaticoduedenectomy): take a little of everything
Endoscopy to look for damage
Chronic pancreatitis
Blockage prevents the normal passage of intestinal contents through the intestinal track (partial or complete)
Types:
-Adhesions: long fiber strips that can clot off
-Intussusception: slips inside of itself and kinks off function
-Volvulus: twist of bowel, kinked, no blood flow, ischemic, necrosis
-Tumor
-Paralytic ileus
-Hernias
intestinal obstructions
Bulge of tissues through a defect in the abdominal wall or musculature. May result in strangulation of tissues and intestinal obstructions. 1. Ventral (incisional) 2. Inguinal: weak abdominal walls with out pouch from lifting heavy things 3. Umbilical: born with it by belly button S/S: Depends on severity of intestinal obstruction Pain Fever so do not give meds for constipation* Constipation Severe abdominal pain Tenderness in the abdomen Vomiting Distended abdomen Redness or discoloration Risks: Obesity Pregnancy Fluid in the abdominal cavity Abdominal surgery Chronic cough Heavy lifting, such as weight lifting. Repetitive straining during urination or bowel movements. Diagnosis: Physical exam, US or abd xray Management: surgery with mesh or bowel resection You may be asked to cough/stand/sit
Hernias
