Exam 2 Flashcards
Anterior Pituitary Gland Hormones
-Growth Hormones
-Proactine (breasts)
-LH (estrogen and progesterone production)
- FSH (testosterone)
-ACTH (goes to adrenal cortex to release cortical hormones)
-TSH (thyroid hormones)
Posterior Pituitary Gland Hormones
-Vasopressin (ADH) in kidneys
-Oxytocin
Hypopituitarism Causes
-Pituitary tumor
-TBI
-Iatrogenic (caused by med intervention)
-Inflammatory conditions (TB)
Hyperpituitarism Causes
Pituitary Tumor
-Prolactinomas most common
-TSHoma least common
Where is adrenal cortex?
Outside of adrenal gland
Mineralocorticoids from adrenal cortext
Aldosterone
-Increases Na+ absorption
-Causes K+ excretion
Glucocorticoids from adrenal cortex
Cortisol
-Affects glucose, protein and fat metabolism, body’s response to stress and immune function
Where is the adrenal medulla?
Inside of adrenal gland
What does adrenal medulla secrete
-Epinephrine
-Norepinephrine
Addison’s Disease Effects
Decreased production of mineralocorticoids and glucocorticoids
leads to decreased cortisol and aldosterone
Addison’s Disease Diagnostic Test
ACTH Stimulation Test (give ACTH, measure cortisol)
1. Cortisol doesn’t rise
-Primary (problem with adrenal glands)
- Cortisol levels rise
-Secondary (problem with pituitary)
Addison’s Disease Symptoms
-Hyperpigmentation of skin
-Low BP, weakness, weight loss
-GI upset
-Vitiligo (pale spots of skin)
Adrenal Crisis Overview
Acute drop in adrenal corticoids d/t sudden discontinuation of glucocorticoid meds or trauma, stress, infection
Adrenal Crisis Symptoms
-Fever
-Syncope
-Convulsions
-Hypoglycemia
-Hyponatremia
-Severe Vomiting
-Diarrhea
Adrenal Crisis Treatment
If Hyperkalemic
-insulin + dextrose
-Thiazide diuretics
-Heart monitoring
If Acidotic
-Bicarb
Cushing Disease
Due to ENDOGENOUS causes of INCREASED cortisol
Cushing Syndrome
Due to EXOGENOUS use of GLUCOCORTICOIDS
Dangers of overusing Prednisone
-Body stops making cortisol
-Overtime, adrenal can atrophy
-When exogenous use stops, body can’t produce its own cortisol –> Adrenal Crisis
Cushing Syndrome Presentation
MOON FACE
BUFFALO HUMP
Thin hair
Double chin
Purple striae
Slow wound healing
Cushing Syndrome Diagnosis
Confirm increase in plasma cortisol levels
Cushing Syndrome Treatment
Meds
-Ketoconazole (corticosteroid inhibitor)
-Mitotane (selective destruction of adrenocortical cells) (monitor for hepatoxicity and hypotension
Chemotherapy or radiation of adrenal gland
Surgery
Cushing Syndrome Surgery
Primary
-Remove adrenal gland
-Monitor for adrenal crisis
-no steroids, adrenal insufficiency
-Seizure precautions
Secondary
-Remove pituitary gland
Thyroid Hormones
T3 and T4
-Overall body metabolism
-Energy production
-Tissue use of fats, proteins, carbs
**Iodine is necessary to make these hormones
Calcitonin
-Inhibits mobilization of calcium from bone
-Recuses blood calcium levels
Hypothyroidism: Hashimotos
-Most common cause of hypothyroid
-Autoimmune: autoantibodies attack thyroid gland —>thyroid unable to secrete T3 and T4
-Women more affected than men
-Mild: generally has vague symptoms and goes undiagnosed
Hypothyroidism: Signs and Symptoms
-Slow metabolism
-Increased TSH but decreased T3 and T4 labs
-Physical Sx: thinning hair, puffy face, thyroid enlargement, constipation, low apatite, fertility issues, menstruation
Cretinism
-Lack of thyroid hormone in children
S/S:
short-stature, mental retardation, coarse facial features, protruding tongue, umbilical hernia
Hypothyroidism Treatment
Meds: Levothyroxine
-Take in morning with food
-Monitor for hyperthyroidism
Myxedema Coma
-Medical Emergency
-Not enough thyroid hormone
Myxedema Causes
-Infection
-Drugs
-Exposure to cold
-Trauma
Myxedema Consequences
-CV collapse
-Hypoventilation
-Hypoglycemia
Myxedema Treatment
-IV drugs (levothyroxine)
-Supportive care
Hyperthyroidism S/S
-Nervous, irritable, insomnia, depression
-Weight loss, hunger, diarrhea
-Fragile finger nails, shaky hands
-Warm moist, skin
-Broken hair/hair loss
-Enlarged thyroid gland
-Increase HR, arrhythmia, HTN
-Muscle cramps, weakness
-Exophthalmos
Graves Disease
-Most common cause of hyperthyroidism
-Autoimmune antibodies —>hypersecretion of thyroid hormones
-More common in women
Graves Disease Labs
-Serum TSH: Decreased
-T3 and T4: Increased
-Thyroid stimulating Immunoglobulins: Increased
-Thyrotropin receptor antibodies
Graves Disease Diagnostic Procedures
Radioactive Iodine Uptake
-Clarifies size and function of thyroid
-Assess for allergy to shellfish or iodine
-ELEVATED UPTAKE= HYPERTHYROIDISM
Graves Disease Treatment
Meds
-Methimazole and propylthiouracil (PTU)
-Thionamides decrease hormone levels prior to surgery
Surgery
-Thyroidectomy
-Radioactive Iodine Therapy
Radioactive Iodine Therapy
Don’t expose others
Thyroid Strom: Acute Thyrotoxicosis
Sudden surge of large amount of thyroid hormone
-Med emergency
-High mortality rate
Thyroid Storm Presentation
-Hyperthermia
-HTN
-Delirium
-Vomiting and abd pain
-Chest pain
-Dysrhythmias
Thyroid Storm Treatment
Treat Hyperthermia
-Tylenol
-Not aspirin–can increase thyroid level
Thionamides to decrease thyroid hormone
Thyroidectomy
Subtotal
-Remove part of gland
Total
-Will need lifelong thyroid replacement
Post-Op
-Support w/ neck pillows
-Monitor airway (laryngeal stridor, risk of edema –>occluded airway)
Thyroid Nodules
Hot Nodules
-Hyperactive nodules
-Not usually cancerous
Cold Nodules
-Hypoactive
-More likely to be cancerous
Parathyroid Overview
-4 pea-sized glands nestled within thyroid tissue
-Produce and secrete Parathyroid Hormone (PTH) in response to hypocalcemia –>breakdown of bone to reestablish normal serum calcium
Hypoparathyroid
-Less common
-Will have s/s of hypocalcemia
-Possible side effect of thyroidectomy
Hyperparathyroid
-More common
-S/S of hypercalcemia
-Surgery is Tx of choice
Pancreas and Diabetes
-Regulates blood sugar
-Beta Cells: secrete insulin to help sugar move into cells
Alpha Cells: secrete glucagon to help convert glycogen into glucose
Metabolic Syndrome
Many Problems that increase risk of DM or CVD
-Obesity
-Insulin resistance
-Sedentary lifestyle
-HTN
-High cholesterol
3 Main Kinds of Diabetes
- Type 1: Autoimmune
- Type 2: Acquired
- Gestational
Type 1 DM
-Autoimmune condition
-Requires insulin for life
-Symptoms begin in childhood
Type 2 DM
-Progressive increased resistance of cells to respond to insulin
-Decreased production of insulin by beta cells in pancreas
-Increased insulin production –> pancreas wears out
Type 1 DM Patient Presentation
-Young and thin
-Quick onset
-Polyuria, polydipsia, polyphagia
-ketones in urine
Type 2 DM Patient Presentation
-obese
-slow onset
-rare to have ketones in urine
Fasting Glucose Levels
Normal: 70-99
Prediabetes: 100-125
DM: 126+
Hgb A1C Levels
Prediabetes: 5.7-6.4
DM: 6.5+
Hyperglycemia S/S
“Hot and Dry, Sugar High”
-Polyphagia
-Polydipsia
-Polyuria
-Dry skin
-Blurred vision
-Delayed wound healing
Hypoglycemia S/S
“cold and clammy, needs some candy”
TIRED
-Tachycardia
-Irritability
-Restless
-Excessive hunger
-Dizziness
Hypoglycemia Management
Glucose <70
-PO 15g fast sugar
-Recheck in 15min–> <70 –> repeat
-Repeat 2-3 times, still low, call Dr.
Glucose Tab
1mg Glucagon IM (activates hepatic conversion of glycogen to glucose)
Glucose <40
-May need IV dextrose
- 1 ampule D50
Hyperglycemia Management
Insulin: short acting
-novolog or humolog
DM Effects
-Slow wound healing
-Blurry vision
-Glycosuria
-Fruity breath
-Rashes on skin, dry/itchy
DM Complications
-Arteriosclerosis
-Peripheral angiopathy (decreased circulation)
-Neuropathy
-Immunosuppression
-Poor wound healing
-DAILY FOOT CHECK
Measures of Renal Function
Serum Creatinine
-Byproduct of protein and muscle breakdown
Creatinine Clearance
-Measures GFR
BUN
-Protein breakdown (liver) urea nitrogen
-Affected by dehydration and steroids
Suprapubic Catheter
-Placed via small incision in abd wall
-Temporary or permanent
Issues
-Poor drainage if cath tip is on wall
-Bladder Spasms: antispasmodics (oxybutynin) Belladonna
Ileal Conduit
Section of ileum for urinary drainage
-Ureters are anastomosed into one end of conduit
-Other end brought out through abd wall to form stoma
No voluntary control, requires ostomy bag
Continent Urinary Catheter
-Intraabdominal urinary reservoir
-Catheterized OR outlet controlled by anal sphincter
-Must self-cath every 4-6hrs
Cutaneous Ureterostomy
-Urinary ostomy
-No control, must have ostomy bag
Nephrostomy Tubes
-Temporary
-Preserves renal function when ureter is completely obstructed
-Cath inserted directly into renal pelvis
-DO NOT CLAMP, compress, or kink
-High risk for infection
Bladder Reconstruction (Neobladder)
-New bladder
-Made from segments of colon
-Urine discharge through urethra
Lower UTI (cystitis)
AKA bladder infection
-usually bladder specific symptoms
Upper UTI
Pyelonephritis=kidney involvement (kidney infection)
-Usually more systemic symptoms
Chronic, asymptomatic UTI
Bacteriuria w/o symptoms
-May not need Tx
UTI Risk Factors
Female
-Short urethra
-close to butt hole
-Sex
-Tight/restrictive clothing
CAUTI
-Most common HAI
-Common E.coli or pseudomonas
Associated with:
-Length of stay
-Health care costs
-Morbidity and mortality
CATH only when necessary
UTI Manifestations
-Dysuria
-Frequency and urgency
-Cloudy, foul smell
-Lower back pain, abd tenderness
Geriatric
-Confusion
-Incontinence
-Anorexia
-Nocturia
UTI Diagnosis
-UA and CA (urinalysis and culture sensitivity)
-Elevated WBC count
-Consider ruling out STI if sexually active
UTI Treatment
-Fluid intake= 3L/day
-Frequent urination (3-4hr)
-Heat to lower abd
-Abx
-Phenazopyridine (decrease dysuria, orange pee)
-Cranberry juice
Pyelonephritis Overview
-Infection and inflammation of renal pelvis, calyces, and medulla
-Usually begin as cystitis
-Common E.coli cause
-Repeat infection may cause scarring
Acute Pyelonephritis
-Active bacterial infection
Can Cause:
-Interstitial inflammation
-Acute tubular necrosis
-AKI
-Abscess
Chronic Pyelonephritis
-Repeated infection, inflammation, and scarring
Can Cause:
-Thickened calyces
-Post-inflammation fibrosis
-Permanent renal tissue scarring
Pyelonephritis Complications
HTN
-D/t destruction of glomeruli
-Renal function decrease –> fluid overload
CDK
-D/t renal fibrosis, scarring, vascular and tubular changes
Sepsis
-Hypotension, tachycardia, fever
Pyelonephritis S/S
-Chills
-Renal colic
-costovertebral angle (CVA) tenderness
-Flank and back pain
-Fever
-Hematuria
Pyelonephritis Treatment
- Increase fluid intake
- Abx
Surgery
-Pyelolithotomy (stones)
-Nephrectomy (kidney)
-Urethroplasty (repair ureter)
Urosepsis Overview
-Sepsis d/t UTI
-Life-threatening: shock, organ failure
Urosepsis Treatment
-Abx
-Increase fluid intake
-Monitor s/s of worsening sepsis: hypotension, tachycardia, oliguria
Nephrotic Syndrome Overview
-Glomerular changes
-Age 2-5
Nephrotic Syndrome Presentation
-Gross proteinuria
-Hypoabluminemia
-Edema (face/eyes —> abd and extremities)
Nephrotic Syndrome Treatment
-Steroids
-Low sodium, potassium, fat diet
-Fluid restriction
-Diuretics
-Albumin
Nephritis Overview
-Ages 2-10
-Post-strep infection
Nephritis Presentation
-Mild edema (face/eyes)
-HTN
-Tea/cola colored urine
-Increase BUN/creatinine
Nephritis Treatment
-HTN meds, diuretics
-Monitor for hyperkalemia
-Low Na+ diet
-Fluid restriction
BPH
Diagnose with PSA
-slight increase
-Major increase could be cancer
Treatment
-TURP (transurethral resection of prostate)
Renal Calculi
-Calcium (most common)
-Struvite (associated with chronic UTI)
-Uric acid (gout, high protein diet)
-Cysteine (least common, d/t metabolic disorder)
Strong familial component, likely to reoccur
Renal Calculi S/S
-Severe pain
-Urinary frequency
-Dysuria
-Fever
-Diaphoresis
-N/V
-Hematuria
-May progress to hydronephrosis
Renal Calculi Diagnosis
-UA
-KUB (x-ray)
-IVP
-CT
-Renal ultrasound
Renal Calculi Treatment
-Opioids
-NSAIDs (ketorolac)
-Antispasmodic (oxybutynin)
-Lithotripsy
-Surgery: stenting, ureteroscopy, urterolithotomy
Renal Calculi Patient Ed
Calcium Stones
-Decrease calcium intake
Limit high protein foods
Uric Acid
-Limit high protein foods, organ meat
Struvite
-Avoid high phosphate food
Polycystic Kidney Disease
-Congenital Disorder (10-15% of CKD)
-Cluster of fluid-filled cysts on nephrons
-Cysts may also develop systemically (heart, liver, intestine, brain)
-Treatment: needle aspiration, transplant
Acute Kidney Injury (AKI) Overview
-Sudden decrease in renal function
-Happens when blood flow is cut off to kidney
AKI Phases
-Onset: initial injury
-Oliguria: kidney insult, 100-400mL urine/day
-Diuresis: begin recovering, not concentrating urine
-Recovery: continues to full function
Prerenal AKI
-Usually d/t decreased renal perfusion
-Shock
-Sepsis
-Hypovolemia
-Nephrotoxic meds
Intrarenal AKI
-Trauma
-Hypoxic injury (thrombosis)
-Chemical Injury (contrast dye, heavy metals, blood transfusion reaction)
-Immunological injury (infection, glomerulonephritis)
Acute Tubular Necrosis (ATN)
Most common intrarenal cause of AKI
-Primarily result of ischemia
-Necrosis, cells slough off, form embolus in renal tubules
-Reversible IF basement membrane is not destroyed
Postrenal AKI
-D/t obstruction below kidney
-Stones, tumor, bladder, BPH, spinal cord disease/injury
AKI S/S
-Fluid overload
-Crackles
-Minimal urine output
-Lethargy, twitching, seizures
-Dry mucus membranes
AKI Treatment
-IV fluids (monitor for fluid overload)
-Diuretics
-Correct electrolyte imbalances
-Temporary dialysis if necessary
Chronic Kidney Disease (CKD) Risk Factors
DM, HTN, HF
Obesity, smoking
Family history
- >60yo
CKD S/S
Neuro: lethargy, slurred speech, tremors
CV: fluid overload, edema, HTN, HF, dysrhythmias
Resp: SOB, crackles, Kussmaul resp, uremic halitosis
Anemia
Osteodystrophy
Uremic Frost
Peritoneal Dialysis
-Instillation of hypertonic dialysate solution into peritoneal cavity
-Dwells for prescribed time, then drained
-Complications: peritonitis, infection
Hemodialysis
-Shunts blood through dialyzer then back into circulation
-usually 3x/week
-monitor continuously
Permanent
-Arteriovenous (AV) Fistula: expect thrill and bruit
-Graft: synthetic vessel
Continuous Renal Replacement Therapy (CRRT)
-24hr dialysis
-Removes uremic toxins
-Acid-base balance and electrolytes adjusted slowly and continuously
Aftercare of Kidney Transplant
-Monitor for infection: lifelong immunosuppressant
-Monitor for organ rejection
1. Hyperacute (within 48hrs)
-Fever, HTN, pain
- Acute (within 2 days)
-Antibody med
Inflammation lysis of kidney - Chronic (gradual)
-Blood vessel injury
-Fibrotic tissue
-Failure
Cardiac Conduction Pathway
- Sinoatrial (SA) node
- Atrioventricular (AV) node
- Down bundle of His –>purkinje fibers
Cardiac Enzymes MI
Myoglobin and CK
-Peak day of MI
CKMB
-Peaks day of MI
Troponin:
-Peaks 2 days after MI
Depolarization
Firing of cells to contract
Repolarization
Recharge for next beat
P Wave
-Atrial depolarization
-Contraction of atria
PR Interval
Time from atrial depolarization to ventricular depolarization
-Norm: 0.12-0.2sec
QRS complex
-Ventricular depolarization (contraction)
-Repolarization of atria hidden in QRS complex
-Want tall and skinny
ST segment
-Represents period between ventricular depolarization and beginning of repolarization
-Norm: isoelectric (flat) and in line with baseline
T wave
-Repolarization
-Norm: upright, smooth, rounded
5 steps for interpretation of EKG
- Rhythm
- Rate
- Assess P waves
- Assess PR interval
- Assess QRS
Rhythm
-Regular or irregular
-Measure R-R
No more than 3 small boxes off
Assess P wave
Is there a p wave before every QRS
Are all p waves same size and shape
Assess PR interval
Beginning of p wave to beginning of QRS complex
Norm: 0.12-0.2sec
Assess QRS complex
-Tall and skinny
-All same
-0.06-0.1sec
Sinus Brady Cardia
HR <60
Causes: Athletes, hypoxia, beta-blockers, digoxin, Valsalva
Symptoms: Syncope, hypotension, confusion, SOB, chest pain
Tx: IV fluids, atropine, O2, pacing
Sinus Tachycardia
HR >100
Causes: Fever, pain, drugs, dehydration, exercise, anemia
Symptoms: palpitations, syncope, chest discomfort, hypotension, restlessness
Tx: Treat what’s causing it
Supraventricular Tachycardia (SVT)
-Rhythm: regular
-Rate: 100-280
-P-waves: cant see
-Pr Interval: can’t calculate
-QRS: tall, skinny, close
Tx: vagal movement, adenosine, cardioversion
Premature Atrial Contractions
-Atria fires before next sinus impulse is due
-Irregular rhythm
-P-waves
-QRS normal
Causes: stress, caffeine, electrolyte imbalance, pulmonary disease
Benign
Atrial Fibrillation (A-fib)
- P-waves
-QRS tall and skinny
-Irregular rhythm
-Main concern: clots
Treatment:
-Anticoagulants
-Meds for rate control: beta-blockers, amiodarone, diltiazem, cardioversion
Atrial Flutter
P-waves: saw tooth pattern
QRS: tall and skinny
Premature Ventricular Contraction (PVC)
-Fire before receiving sinus impulse
-Irregular rhythm
-Electrolytes: Hypokalemia, hypomagnesia
-Treat underlying cause
Ventricular Tachycardia (vtach)
-No p-waves
-QRS: tall and wide
-Life Threatening
-Assess Pt: do they have a pulse
-Treatment: CPR and DEFIBRILATION
Ventricular Fibrillation (Vfib)
-No p-waves
-QRS: not discernable
-No pulse b/c no cardiac output
-Treatment: CPR and DEFIBRILATION
Torsades de Pointes
-Classic Twist: polymorphic ventricular tachycardia
-Irregular, 150-250bpm
-Need magnesium sulfate via IV
-P-wave absent
-QRS irregular
-Defibrillate
1st Degree Heart Block
-Delayed conduction through AV node
-Only treat if symptomatic
2nd Degree Heart Block
-Intermittent AV node blockage
-Missing beat
3rd Degree Heart Block
-Atrial and ventricular disassociated
-Must have pacemaker
Stenosis
Narrow valve opening
Regurgitant
-Leaky valve that doesn’t close completely
Causes of Valvular Dysfunction
Congenital
Acquired
-Degenerative: age, HTN, atherosclerosis
-Rheumatic: gradual fibrotic change and calcification
-Infective Endocarditis: infection destroys valve (strep)
Expected Findings of Valvular Dysfunction
Murmurs
Aortic or Mitral Valve Dysfunction can cause:
-LV hypertrophy
-decreased CO
-Orthopnea
-Paroxysmal nocturnal dyspnea
-Fatigue and weakness
-JVD
Mitral Stenosis
-Narrow mitral valve
-S/S: pulmonary edema, decreased perfusion
Mitral Insufficiency
-Not closing completely
-Blood flows back into atrium
-Decreased blood to aorta
-S/S: fatigue, weakness, dizzinessMi
Mitral Valve Prolapse
-Valve flipped inside out
-Many times asymptomatic
Aortic Stenosis
-Too narrow
S/S: decreased perfusion, SOB, fatigue, dizziness
Pericarditis
-Inflammation of pericardium
Pericarditis Causes
-Follow respiratory infections
-MI
-Exacerbation of a systemic connective tissue disease
Pericarditis Presentation
-Chest pain
-Pain breathing, coughing, swallowing
-PERICARDIAL FRICTION RUB
-SOB
Pericarditis Treatment
NSAIDs
Cardiac Tamponade
-Complication of inflammation of heart condition
-Fluid accumulation in pericardial sac
Cardiac Tamponade Presentation
-Dizziness, dyspnea
-Dextriade: hypotension, muffled heart sounds, JVD
-ECG
PULSUS PARADOXUS: SBP decrease >10mmHg during inspiration
Cardiac Tamponade Treatment
-Pericardiocentesis
Myocarditis
Inflammation of myocardium
Can lead to HF
Myocarditis Causes
-Viral, fungal, bacterial infection
-Systemic Disease (Chron’s)
Myocarditis Presentation
-Can be asymptomatic
-Tachycardia
-Murmur
-friction rub
-cardiomegaly
-chest pain
-dysrhythmias
Rheumatic Endocarditis
-Infection of endocardium d/t complications of rheumatic fever
Rheumatic Endocarditis Causes
-Preceded by group A beta-hemolytic streptococcal pharyngitis
-Produces lesions in heart
Rheumatic Endocarditis Presentation
Fever
chest pain
joint pain
tachycardia
SOB
rash on trunk/chest
FRICTION RUB AND MURMUR
muscle spasms
Infective Endocarditis
Infection of endocardium (valvular dysfunction)
Infective endocarditis Risk Factors
-Cardiac devices (pace maker)
-Structural cardiac malformation
-Invasive Procedures (dental, piercing, tattoo)
-Drug use (effects tricuspid)
Infective Endocarditis Presentation
Fever
Murmur
Petechiae
+ Blood cultures
Splinter hemorrhages (red streaks on nails)
**Monitor for s/s of resp distress
Diagnosis for Infective heart disorders
Positive blood cultures
Diagnosis for rheumatic endocarditis
Throat swab
Diagnosis for pericarditits
Cardiac enzymes present
Cardiac Inflammatory Markers
ESR, CRP
Patient care for: Pericarditis, Cardiac Tamponade, Myocarditis, Rheumatic Endocarditis, and Infective Endocarditis
-Auscultate heart sounds
-O2
-Monitor VS
-Meds: Abx, NSAIDs (pericarditis not myocarditis), Prednisone
-Pericardiocentesis
-Valve debridement for endocarditis
Patent Ductus Arteriosus (PDA)
-Pulmonary artery and aorta still connected
Tx: Endomethasen, NSAIDs
-Inhibit prostaglandin to help close
Atrial Septic Defect (ASD)
-Opening between L+R atrium
-Fix with surgery
-More blood to lungs
Ventricular Septal Defect (VSD)
Opening between L+R ventricle
-More blood to lungs
-Fix with surgery
Tetralogy of Fallot (TFT)
Defects:
1. Pulmonary stenosis
2. Thickened right ventricular wall
3. Ventricular septal defect
4. Aorta overrides septal defect
-Decreased blood flow to lungs
-Wait 2-6mo to do surgery
Coarctation of Aorta
Increased pressure on heart, hypertrophy, decreased systemic perfusion
-Arch of aorta is narrow
-Backs up into LV
S/S: pallor, dyspnea, heart megaly, hepatomegaly, decreased peripheral pulse and cap refill
Tx:
-Prostaglandin (keeps ductus arteriosus open)
-Beta-blockers
-Balloon angioplasty
Causes of HF
-HTN
-MI
-Pulmonary HTN
-Dysrhythmias
-Valve problems
-Pericarditis
-Cardiomyopathy
Left Sided HF
-Systolic (can’t pump)
-Diastolic (can’t fill)
Right Sided HF
D/t chronic lung condition
Left Sided HF Overview
-Can’t pump blood forward
-Less blood reaches tissues
-Blood backs up –>fluid build-up in lungs
Left Sided HF Presentation
-Dyspnea
-Orthopnea
-Fatigue
-Displaced apical pulse d/t hypertrophy
-S3 gallop
-PULMONARY CONGESTION
-Frothy-pink sputum
Right Sided HF Overview
-Not pumping blood to lungs
-Blood accumulates in body
If occurring by itself, may be d/t respiratory problem: Cor pulmonale
Right Sided HF Presentation
-JVD
-Edema
-Ascites
-Fatigue/weakness
-Nausea
-Anorexia
-Polyuria
-Hepatomegaly and tenderness
HF Diagnostics
BNP
300 mild, 600 mod, 900 severe
Ejection Fraction (blood pumped from LV on beat):
55-70% normal
<40% HF
Labs for HF
BNP
CBC
BMP
CMP
Nursing Action HF
-O2 if needed
-High fowlers
-Energy conservation
-Low sodium diet
-Possible fluid restriction
Meds for HF
-Diuretics
-Afterload reducing agents
-Inotropic agents
-Beta-blocker
-Vasodilators
-Human B-type natriuretic peptides
-Avoid NSAIDs
Acute Pulmonary Edema: Complication of HF
-Life threatening emergency
Presentation
-Anxiety
-Tachypnea
-Respiratory distress
-Dyspnea at rest
-Change in LOC
-Fluid in lungs
Tx
-High Fowler’s
-HIGH FLOW O2
-IV morphine
-IV diuretic
-ABG electrolytes
-Fluid restriction
HTN Findings
“silent”
-Headache, flushing, dizziness, fainting, retinal changes, nocturia
HTN Meds
-Diuretics
-Calcium channel blockers
-ACE inhibitors
-ARB
-Aldosterone receptor blockers
-Beta blockers
-Central A2 agonists
-Alpha adrenergic antagonists
Hypertensive Crisis
Presentation
-Headache
- >180/120
-Blurred vision, disorientation, dizziness, Epitaxis (nose bleed)
Tx:
-Iv antihypertensive (nitroprusside, nicardipine, labeltalo)
-BP every 5-15min
-Assess neurological status
CAD Overview
Most common cause: atherosclerotic plaques
Umbrella including:
-Angina
-ACS (acute coronary syndrome): decreased coronary blood flow
-MI
CAD Risk Factors
Non-mod
-age, gender, race/ethnicity, family hist
Modifiable
-HLD, Smoking, HTN, Obesity, DM, stress, diet, renal disease, OCP/ HRT (birth control and hormone therapy)
CAD Manifestations
-Chest pain: crushing, squeezing, tight, elephant on chest
-Dyspnea, tachypnea
-Pallor, mottling, diaphoresis
-GI distress
-Anxiety, fear, sense of doom
Pharm Therapy for CAD
Nitrates (nitroglycerin) and morphine (pain control)
Beta-blockers
Calcium channel blockers (nifedipine, amlodipine)
Statins (lower cholesterol)
Thrombolytics (reteplase), heparin, aspirin: to thin blood
Antidysrhythmic and Vasopressors
-Amiodarone, lidocaine, propranolol
-Dopamine, norepinephrine, levophed
Non-Pharm Intervention CAD
-PCI/PCR
-CABG
-Intra-aortic balloon pump (increases stroke volume)
-Ventricular Assist Device (partial or complete control of cardiac function)
Coronary Artery Bypass Graft (CABG)
-Grafts vessel from leg or synthetic vessel
-Bypasses blockage
-Less preferred than PCI
Nursing Care:
-Chest tube management
-Pain control
-Monitor hemodynamic status
-Monitor for infection
-I and O
-Incentive spirometer
-Splint for cough
PAD Symptoms
“silent”
-Pallor
-Palpable coolness
-Pain (intermittent claudication) –[pain with exercise]
-Paresthesia
-Weak/nonpalpable pulses
-Loss of hair
-Thick toenails
-Common with DM
Arterial Ulcers
-Ischemic wounds develop d/t lack of blood flow
-Extremity pale and weak pulses
-Wounds are “dry” as opposed to venous ulcers that “weep”
-Pain INCREASES when extremity is elevated, LOWERED when lowered
Nursing Care PAD
-Increase exercise slowly
-Promote vasodilation (warm environment)
-No restrictive clothing
Meds
-Antiplatelet (aspirin)
-Statin
Procedures
-Percutaneous transluminal angioplasty
-Grafts
-Atherectomy
Compartment Syndrome
-Tissue pressure within a confined space that restricts blood flow
-Results ischemia and tissue death
6 Ps
-Pain, pressure, paralysis, paresthesia, pallor, uselessness
Tx: fasciotomy
DVT
Virchow’s Triad: Venous stasis, venous injury, hypercoagulability}increase clot risk
Tx:
-Anticoagulation: heparin
-Surgery
-Filter placement
S/S:
-Redness, warmth, tenderness, ropiness, swelling
