Health Deviations

Renal

100

What is the four stages of ARF?

initiating, oliguric, diuresis, recovery

200

What are the causes of ARF? and explain them

Pre-renal-happens before the kidneys like hemorrhage, decreased cardiac output, vasodilation, hypoperfusion Intra-renal-happens at the kidney, most common is ATN. direct damage to renal tissue, impaired nephron function Post-renal- obstuction of urinary tract, renal calculi

300

What are the progression of CRF? and Explain what happens in each stage.

Reduce Renal Reserve- kidney function normally, Bun is in high normal and S/S are not dicernable. Renal Insufficiency- GFR falls 40-70, mild azotemia, BUN increases, impaired urine concentration. olguria, mild anemia, decreased bicarb Renal Failure- GFR decreases 60-40, severe azotemia, acidosis, hypernatremia, hyperkalemia, hypocalcemia, hyperkalemia, increases triglycerides, hyperphosphatemia, increase BUN & CR End Stage Renal Failure- GFR <15, 90% of nephrons are destroy, BUN & CR Soar, cannot maintain fluid and elctrolyte balance. oligure < 500mls/day, uremic syndrome.

400

What are the Stages of CRF?

1.slight kidney damage with normal or increase filtration GFR more than 90 -mild decrease in kidney function GFR 60-89 -moderate decrease in kidney functioin GFR 30-59 -severe decrease in kidney function GFR 15-29 -kidney failure requiring dialysis or transplantation Less than 15

500

What is Uremic Syndrome and name one complication from each system.

SEE Powerpoint

CHF

100

Name the Types of Heart Failure.

Systolic (L sided) Diastolic (R sided) Chronic Acute

200

Differintiate between Systolic and Diastolic Failure

Systolic- inability of heart to pump Cause: HTN, cardiomyopathy, MI, valvular heart disease Results in EF < 45% Diastolic- Inability of heart to relax Causes: L ventricular hypertrophy, aortic stenosis, hypertrophic cardio myopathy EF is normal- 55%

300

Differintiate between Pre Load and After Load

PRELOAD- the degree of myocardial fiber stretch at the end of ventricular filling or diastole. increased preload to a point is positive and increases CO. that is, stretching the fibers during diastole increases force of contraction duing systole. overstretching of the fibers-> decreased cardiac output AFTERLOAD-amount of wall tension (pressure) the ventricle must develop during systole to eject blood againist the peripheral resistance. factors which affect afterload include: intravascular size of radius, aterial pressure. Note: ventricular hypertrophy (a pathologic consequence of failure) can decrease afterload r/t increased muscle mass -> increased work of ejection

400

Name S/S of R sided HF (diastolic) and L sided HF (systolic)

R sided- Jugular Vein Distention, hepatomegaly, splenomegaly, vascular congestion of the GI tract, Peripheral/ dependent edema, Mumurs, Weight Gain, Increase HR, Ascites, Anasarca, Upper Quad pain, Anorexia L sided- increased HR, PMI displaced, Crackles, s3 and s4 heart sounds, restlessness, confusion, weakness/fatigue, dyspnea, orthopnea, dry hacky cough, nocturia, pink frothy sputum.

500

Differnitiate between Acute decompensated HF and Chronic HF. Give Cause and S/S

Acute- compensatory mech fail quickly, manifests as pulmonary edema, can be life threatening, caused by L ventricular failure typically d/t CAD. S/S are SOB, tachypenic, poor ABGs, anxiety, wheezing/crackles, coughing, pink-frothy sputum. Chronic-characterized as progressive worsening of ventricular function that results in ventricular remodeling (change in size, shape, or function), comp mech fail over time, can have S/S of both R and L sided HF. classified into stages. A-D

Respiratory Adult

100

What is CorPulmonale?

• COPD complication results from pulmonary hypertension which is caused by dx affecting the lungs or pulmonary blood vessels. LATE MANIFESTATION OF COPD. Once pt develops this the prognosis worsens.

200

What is COPD? PATHO, LAB Test/results, and causes?

• Causes: emphysemia or chronic bronchitis • Test: o Diagnosis is confirmed by spirometry whether or not the pt has chornic symptoms o X-ray o Exercise test to determine O2 saturation in the blood and pulse oximetry o ECG can show signs of right ventricular failure • Lab values: Typical findings include reduced FEV/FVC (forced vital capacity) and increased residual volume and total lung capacity. • Pulmonary function tests would typically reveal decreased FEF (forced expiratory flow) and decreased FEV (forced expiratory volume • Patho: o Characterized by presence of airflow obstruction; either airflow problem or alveolar problem o Infection if major contributing factor to the aggravation & progression of COPD o a-Antitrypsin(ATT) deficiency is the only known genetic abnormality that leads to COPD

300

Differnitiate between Emphysema and Chronic Bronchitis and S/S of both

Emphysema-pink puffer Bronchitis- Blue bloater See PP

400

if a person has these ABGs which respiratory dx is this COPD, Emphysema, or Chronic Bronchitis? ABGs pH-7.3 Pao2-60 Pco2-50 Hco3-30

COPD

500

Describe the process (progression) of ARDS and stages

Trauma- what occurs that causes ARDS- (asphyxia, aspiration, septicemia. Pulmonary emboli, pneumonia. Cause leads to cascade of effects, diminish blood flow through aveolar capillairies systemic inflammatory response this causes damage to the capillaries. This can have hemorrhage, capillary leakage (increased permeability), thrombi formation resulting in interstitial edema. The alveoli fill with fluid This interferes with surfactant activity (this is the substance that decreased surface tension in the expansion of the alveoli) Decrease surfactant causes the alveoli to stick together (the alveoli cannot inflate) Pulmonary edema NO GAS EXCHANGE CAN OCCUR

Respiratory Infant

100

What is TTN?

• Also called RDS type II • Risk factors: c-section birth w/out, asphyxia, maternal analgesic, maternal diabetes • Pathophys: infant can’t clear lungs of fluid, mucous or debris or they aspirate amniotic fluid, delayed absorption of fetal lung fluid • S&S: at birth-normal resp rate. However, within hours after birth- expiratory grunting, nasal flaring, mild cyanosis, & resp rate as high as 120

200

What is Medistinal Shift?

• Air gets into lungs is then trapped leading to alveolar hyperinflation & possible rupture. It this continues to progress a pneumothorax (collapsed lung) or mediastinal shift (air in the thoracic cavity pushes from the affected side over to the “good” side & interferes further w/ gas exchange) may occur

300

What are the Cause of Respiratory Distess in the Newborn?

prematurity asphyxia ID (infants of diabetic mothers) C-Section other maternal and fetal factors

400

Name the PATHO and S/S of RDS

• Patho: insufficient surfactant-alveoli collapse w/ot surfactant & lungs become stiff & incompetent – hypoxia occurs; causing pulmonary vasoconstriction & decreased blood flow to lungs-resulting in possible resp failure &/or return to fetal circulation • S&S: increased cyanosis, or pallor & motting, tachypnea, apea, grunting resp or dyspnea, nasal flaring, significant sternal & intercostal retractioins, inspiratory rales, rhonci, HR may be WNL, hypothermia r/t poor metabolism associated w/ low O2 levels, flaccid, hypotonic muscles, unresp to stimuli, or hypertonic &/or seizures depending on CNS damage

500

What are the S/S of Meconium Aspiration in utero, at birth, and after resistation?

See PP

Suprise Me

100

What causes Meconium Aspiration?

Asphyxia-may cause the fetus to pass meconium

200

if the pt is in the diuretic phase of ARF the nurse must monitor for which electrolyte imbalances? A. Hyperkalemia and Hyponatremia B. Hyperkalemia and Hypernatremia C. Hypokalemia and Hyponatremia D. Hypokalemia and Hyponatremia

D. hypokalemia and hyponatremia

300

Name the Compensatory Mechanisms for CHF and some things from each

increased SNS activity Hormonal response dilation and ventricular hypertrophy

400

A compensatory mechanism involved in HF that leads to inappropirate fluid retention and additional work load of the heart is. A. ventricular dilation B. Ventricular hypertrophy C. Neurohormonal Response D. SNS activity

C. Neurohormonal Response

500

Name Lab Results associated with CRF stages and the causes

See breakdown, PP