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NUR EXAM ONE STUDY GUIDE
o NS is a condition of increased glomerular permeability
that allows larger molecules to pass through the membrane into the urine and then be excreted.
o Immunological Kidney disorder
o This causes massive loss of protein in the urine,
edema formation, and decreased plasma albumin levels.
▪ Proteinuria- severe protein loss more than 3.5 g in
hour urine sample.
o Key features:
▪ Massive proteinuria >3.5g / 24hrs
▪ Hypoalbuminemia <3g/dL
▪ Edema (facial and periorbital)
▪ Lipiduria
▪ Hyperlipidemia
▪ Increased coagulation (renal vein thrombosis)
▪ Reduced kidney function (↑ BUN, ↑ Cr, ↓ GFR)
o Treatment- immunosuppressant agents (if immunity
based).
▪ ACE inhibitors (to decreased protein loss in urine & ↓BP)
▪ Statins (improve blood lipid levels).
▪ Heparin (↑ coagulation / risk of thrombosis → treat
vascular effects and improve kidney function)
o Diet:
▪ If GFR is normal- dietary intake of complete proteins
is needed
▪ If GFR is decreased- dietary protein is decreased,
diuretics and sodium restriction.
o AKI is rapid reduction in kidney function resulting in a
failure to maintain fluid and electrolyte balance, and acid-base balance.
▪ Can occur over a few hours or days
o Severity of AKI is based on serum creatinine increase,
and decreased urine output- an increase in specific gravity (meaning urine is more concentrated or the patient is dehydrated).
o GFR isn’t used to measure acute injury or illness—
only chronic kidney disease.
o 3 types of AKI
▪ prerenal - conditions that reduce blood flow /
oxygen to the kidney → decreased perfusion to
kidneys
- azotemia- nitrogenous waste/toxin build up
o effects LOC, mood, change in personality
o Kidney stones
o Blood clots in urinary tract
o Neurogenic bladder →Nerve damage
o Mean atrial pressure is important in determining
adequate kidney perfusion!!!
▪ MAP= (systolic+ 2[diastolic])/
Mean atrial pressure of 65 is needed to perfuse the kidney!! ➢ Manifestations (s/s) of AKI o Oliguria o Fluid Volume Overload ▪ Crackles ▪ Edema ▪ Anasarca (generalized edema) ▪ ↓ 02 sats ▪ ↑ RR o LOC changes o Labs (↑BUN, ↑Cr, urine specific gravity >1.030)
o Nursing considerations / Interventions for AKI:
▪ Prevention is key! - urge patients to drink 2-3 L
of water daily.
- Monitor Fluid status (I&O, weight, ↑ hydration,
characteristic of urine)
- Report Output <0.5mL/kg/hr if persists >2hr
<30mL/hr
- Monitor for kidney functions
o Labs (BUN, Cr, GFR, electrolytes, osmolarity)
o I&Os
▪ You want output to be more than input ▪ Sodium, potassium, and specific gravity determine hydration status.
o Contrast dyes
o MAP > 65 mmHg
- Diuretic therapy- happens after AKI is
starting to be resolved! (Releasing extra fluid through the urine - This is a good sign!!! - Watch for dehydration! - Its normal to have fluids hanging during the diuretic phase! - Titrate fluids!)
o Low protein
▪ Because protein molecules are huge and put on the strain to process
o Low sodium
▪ Since the body has high sodium concentration due to AKI
o effects of CKD on the kidneys:
▪ decreased urinary output
- urine output decreases as the patient progresses through CKD until they reach oliguria ▪ increased potassium, BUN, Creatinine
- put patient on tele monitor if they are in hyperkalemia!!! ▪ Decreased GFR ▪ Maintains homeostasis until late signs ▪ Salt wasting:
- In early stages of CKD patients will lose the sodium and the water won’t follow!! So, excess fluid and hyponatremia
- In late stages CKD- no urine output so salt and water stay and hypernatremia occurs!
o Metabolic changes of CKD:
- Urea and creatinine build up
- Hyponatremia- early stages
- Hypernatremia- late stages
o Hyperkalemia- late stages → due to
kidneys not excreting potassium though the urine.
o Metabolic acidosis occurs due to lack of
urine excretion, and the body becomes more acidic! → kussmaul respirations! (deep rapid resp) → pt is compensating!
o Patient is normally in a slight acidic
state all the time.
o Effects of CKD on the body:
▪ Cardiac-
- Hypertension
- Hyperlipidemia
- Heart failure
- Crackles
- Pulmonary edema (pink frothy sputum)
- Tachypnea
- hyperpnea
- Pericarditis, cardiac tamponade ▪ Integumentary
- Uremic frost! - causes patient to be itchy!
o Keep cold
o Tepid water
▪ Hematological
- Anemia (fatigued, SOB) →from lack of RBCs → from Ø erythropoietin
o Put on fall precautions!!!-
orthostatic hypotension ▪ Musculoskeletal
- Bone pain
- Muscle weakness
- Pathological fx (↓Ca) ▪ Gastrointestinal
- Stomatitis- huge ulcers in the mouth
o Patient won’t want to eat
o NG tube
- PUD- GI bleeds
- Uremic Fetor
o Dietary restrictions of CKD
▪ Depends on the severity of the CKD and how well their kidneys are function
o Restriction early during the disease
prevents complications of CKD, and preserves kidney function (↑ for dialysis) Monitor BUN and Albumin
o Lay patient supine and let rest, BP
should go back to normal. ▪ Vascular access devices:
o AV fistula (artery to vein)
o AV graft (plastic loop)
- Temporary (less than 6 months)
o HD catheter
o Ports
▪ AV fistula
- Doctor stitches an artery and a vein together.
o Puts arterial blood back into vein and
it gets huge!
o Takes weeks for it to get big and
allow for hemodialysis!
o “feel the thrill”
▪ bruit- sound of the swooshing of the blood ▪ thrill- feel the vibration with your fingers
- DO NOT UNDER ANY CIRCUMSTANCES USE THE AV FISTULA ARM FOR ANYTHING BUT DIALYSIS!
o No BP, IVs, Phlebotomy- nothing!
o Any stress to this arm can blow the fistula
- Nursing care for AV fistula
o Palpate and auscultate- bruit and thrill
o Distal pulses
o ROM- helps form the fistula
o No heavy lifting or carrying
o No pressure
o Watch for infection → complication
o Aneurysm can form at AV fistula
site → complication ▪ Dialysis disequilibrium syndrome → Complication
- Life threatening!
- → occurs if you pull off the fluid too fast!
- s/s: restless and headache, decreased LOC, seizures, coma, death
- give barbiturates and anticonvulsants- standing order
- Watch for change in mental status
- Call a rapid immediately!!!
o Peritoneal dialysis
▪ Allows the exchange of wastes, fluid and electrolytes to occur in the peritoneal cavity! ▪ Sterile procedure- catheter placed in the abdomen into the peritoneal cavity.
- Never do anything to the port without cleaning it first. ▪ Home dialysis ▪ Fill, dwell, drain.
- Number of exchanges depends on doctor prescription. ▪ Complications:
- Peritonitis
- Pain
- Exit site infection
- Poor dialysate flow
o Kink
o Put drainage effluent further away
o Hang intake bag higher
o Let gravity do the work
- Dialysate leakage
- Bleeding at site
- Bowel perforation ▪ Warm up the dialysate by using heating ▪ Same nursing considerations as HD- vitals, weight, etc.
- Cirrhosis- liver transplant is only cure
o Remember liver functions:
▪ Produces bile ▪ Produces coagulants ▪ RBCS ▪ Clotting factors ▪ Metabolites and filters everything PO.
o Cirrhosis- extensive, irreversible scarring of the liver,
usually caused by chronic reaction to hepatic inflammation and necrosis ▪ Progressive – develops slowly ▪ Alcohol is number 1 cause. ▪ If liver isn’t functioning properly, toxins will build up in the blood.
o Causes of cirrhosis:
▪ Alcohol liver disease ▪ Viral hepatitis (normally hep C). ▪ Autoimmune hepatitis ▪ Drugs and chemical factors- acetaminophen and anything else that’s hepatotoxic ▪ Gallbladder disease- biliary cirrhosis ▪ Metabolic/genetic cause
o Lactulose- binds the ammonia in bowels
and is excreted ▪ Risk factors for Hepatic Encephalopathy
- High protein diet → protein breaks down to nitrogenous waste → elevated ammonia
- Infection
- Hypovolemia
- Hypokalemia
- Constipation or GI bleed
o End stage cirrhosis physical assessment:
▪ Ascites ▪ Jaundice
- Teach patient that using cool water instead of warm water for skin irritation and don’t use a lot of soap. Lotion can soothe as well! ▪ Coagulation problems ▪ Fatigue ▪ Confusion/memory loss- encephalopathy ▪ Spider angiomas ▪ Rash/dry skin
- Worry about skin integrity! ▪ Petechiae/ecchymoses- due to clotting factors ▪ Palmar Erythema ▪ Liver flaps (asterixis)
- Hands flapping almost like a tremor, comes and goes ▪ Gynecomastia & impotence
o Complications to cirrhosis:
▪ Portal hypertension- leads to splenomegaly, ascites, and esophageal varices
- Persistent pressure in portal veins → backs up → leads to varices
- Blood backs up into spleen- splenomegaly.
o Platelets can’t get into the blood-
bleeding risk!!!
- Esophageal varices+splenomegaly = HUGE bleeding risk- patient will more than likely die ▪ Ascites- the collection of fluid in the peritoneal cavity caused by increased hydrostatic pressure from portal hypertension.
- Abdomen will be hard, tight, and tender- if you roll the patient from side to side you can hear a swooshing sound
- Monitor F & E,
- ↓Na diet
- Diuretics
- Paracentesis is necessary to get rid of fluid if diuretics are no longer working.
o It is important to have client void their
bladder before undergoing the procedure, to ensure bladder is out of the way and won’t get punctured!
o Patient positioned up right. (fowler’s
position in bed)
- Prevent and monitor for Resp. complications ▪ Esophageal varices- result of portal hypertension
- Life-Threatening!
- Varices occur when fragile, thin-walled esophageal veins become distended and tortuous from increased pressure.
- If they burst and bleed it is life threatening- the massive blood loss results in hypovolemic shock bad liver = ↓ to Ø clotting factors
- Monitor for melena & hematemesis ▪ Biliary Obstruction - ↓ production of bile
- Fat soluble vitamins are malabsorbed.
o Vitamin K is fat soluble and is
responsible for clotting factors!
o Loss of clotting factors = bleeding
o Treatments of cirrhosis:
▪ Transplant is only cure
- No alcohol! - you will not get on transplant list if you continue to drink. ▪ Diet:
- Small frequent meals (5-6/day)
- High protein unless have hepatic encephalopathy
- High carbs
- Moderate fats
- Moderate vitamins ▪ TPN- total parental nutrition- only given through central line!
- Due to high concentration of glucose
- Check blood sugar!
- Watch for encephalopathy ▪ PPN- partial peripheral nutrition
- Can go into peripheral line
- Due to glucose being cut in half.
o Nursing considerations / interventions of cirrhosis:
▪ Medications:
- Diuretics- ascites
- PPI/H2 blockers- NEVER BOTH AT THE SAME TIME!
▪ CAT scan first
- Rule out cancer ▪ Lab results
- Elevated lipase and amylase
o 3x normal amount
o main diagnostic!
- Elevated WBC and Sed Rate
o Due to inflammation and
infection of necrotizing pancreas
o Due to fluids shift
o Assessment:
▪ Jaundice skin ▪ Gray-blue skin on abdomen/flank areas
- Cullens’ sign – “C” shaped bruising around umbilicus
- Turner’s sign- bruising on flank
- This is a very bad sign and you need to call PHCP!!!!
- Leaking enzymes is causing the pancreas to hemorrhage ▪ Guarding and rigidity-LUQ
- May have no bowel sounds LUQ- NPO IMMEDIATELY ▪ Ascites
- Due to splenic HTN ▪ Pt found in fetal position
- Best for alleviating pain ▪ Palpable mass
- Pancreatic pseudocyst
o Be careful not to rupture it!
- Can be drained
- Can rupture and hemorrhage ▪ Vital signs
- Elevated temp
- Tachycardia
- Hypotension
o If these happen at the same time
CALL A RAPID!
▪ Monitor for respiratory distress
o Treatment:
▪ Manage Pain!!
- NPO! - (↓work of the pancreas = ↓inflammation)
- IVF
- H2 blockers & PPIs ▪ NG Tube insertion with suction
- Gastric decompression
- Opioids for pain management
- Monitor for s/s of Hypocalcemia!
- Chronic Pancreatitis
o Progressive, destructive disease of the panaceas
that has remissions and exacerbations ▪ During exacerbations, the treatment is the same as acute pancreatitis
o Causes:
▪ Alcoholism is # ▪ Chronic obstructive CBD- choleylithisis ▪ Autoimmune ▪ Idiopathic- unknown cause
o Signs and symptoms:
▪ Pain in upper abdomen-LUQ
- Burning and gnawing
- Less intense than acute ▪ N/V- NG tube ▪ Unexplained weight loss ▪ Muscle wasting ▪ Signs of diabetes mellius
- 3 Ps
o polyuria
o polydipsia
o polyphagia
- this is due to lack of insulin production.
- This is number one sign of upcoming exacerbation ▪ Ascites- due to splenic HTN ▪ Fatigue ▪ Dark urine ▪ Steatorrhea stools (chronic only)
o Pancreatic Enzyme Replacement Therapy “PERT”
▪ Pancrelipase & Creon
- Take with all meals and every snack
- Full glass of water
o Nutritional; support
▪ NG tube and NPO ▪ TPN
- Watch blood sugar since TPN is high in glucose ▪ High carbs & Hi protein - No lipids! ▪ Tolerated diet in healing phase (chronic on bland diet all the time)
- Small, frequent meals
- Low fat
- Bland diet
- No caffeine, alcohol or lipids!
▪ Cancers
o Body’s defense mechanism for a trauma
▪ Releases anticoagulants and clotting factors all at the same time
o Assessment & S/S
▪ Pain ▪ CVA like symptoms ▪ Dyspnea ▪ Tachycardia ▪ Bowel necrosis ▪ ↓ renal function
o Labs will show
▪ Prolonged PT/PTT ▪ ↓ platelets (<50) ▪ ↓ fibrinogen (<100) ▪ + D-Dimer (>4 suggests DVT)
o Treatment
▪ Treat underlying cause
- Reduce infection
- Correct shock, acidosis ▪ Heparin to limit clotting ▪ When progressed – give RBCs and FFP
- Hemodynamic Monitoring
o Purpose : more accurate measurement of vascular
capacity, blood volume, pump effectiveness and tissue perfusion.
o Swan-Ganz catheter- pulmonary artery catheter
▪ Central venous pressure (CVP)
- 4-12 is normal range
- Reflects amount of blood returning to the heart and the ability of the heart to pump the blood back to arterial system - a measure of blood volume and venous return
- primarily used to assess fluid volume status
o decreased= hypovolemia
o increased=fluid volume overload RHF?
▪ Arterial line
- Gives constant BP ▪ pulmonary artery wedge pressure (PAWP)
- or just wedge pressure ▪ cardiac output (CO)
- HRxSV
- 4-7L/min
- amount of liters the heart can pump in one minute
- Acute Coronary Syndrome
o Unstable Angina
▪ Chest pain at rest – not relived with nitro ▪ ↑ number of attacks and severity
▪ > 15 min duration
▪ ST changes, negative troponin &/or CK levels ▪ Sudden onset o PQRST of pain assessment:
▪ Provoking- at rest? Or activity? (does it change with breathing?) ▪ Quality- what type of pain (sharp, dull, squeezing) ▪ Radiating ▪ Severity- rate ▪ Timing- how long
o Acute myocardial Infarction
▪ >40% blockage o CAD health considerations ▪ Women:
- Postmenopausal women 2-3x more likely than
pre
o Indigestion
o Chronic fatigue o Inability to “catch their breath” o Aching o Choking / strangling
- ST elevated Myocardial Infarction (STEMI)
o Ruptured atherosclerotic plaque → thrombus & platelets
aggregate at site → 100% occlusion to coronary artery (ischemia → injury/onfarction)
o T waves & P waves should ALWAYS be in same direction
o An Inverted T wave → Ischemia! o ST segment elevation → muscle injury (Active heart attack) o Long Q wave → infarc’d o Clinical Manifestations / S&S of MI
▪ Pain (crushing) to jaw, back, shoulder, abd ▪ N/V ▪ Diaphoresis ▪ Dyspnea ▪ Dizziness & fatigue ▪ WBC’s may ↑ After MI in response to necrotic tissue ▪ S3 → very First sign of HF
o Interventions
▪ Hook up to 12 lead EKG
- Gold standard- within 10 minutes!!!!
