PAMPASABOG NG BUNGO!!! Bleh!!! Hahahahaha!!!

Kaya mo yan!!! 
~ Sir Melted

RHEUMATIC HEART DISEASE

Causative agent: Group Beta Hemolytic Streptococcus  Pharyngitis

Major signs
Joint inflammation  migratory polyarthritis
(heart) inflammation  carditis
Nodules  subcutaneous nodules; painless
Erythema marginatum  rash with red lining
Sydenham’s chorea  involuntary jerking of extremities (St. Vitus’ Dance)
Minor signs
Sore throat within the last 5 weeks
Temperature > 38.5 degree Celcius
Rhinitis
Elevation of WBC(marker of i4nfection) and ESR(marker of inflammation)
Positive ANA test (marker of autoimmunity)

Diagnosis: 2 major signs Jone’s Criteria

1 major sign + 2 minor signs

Treatment: Antibiotic Therapy

Initial treatment: Penicillin, oral, 10-14 days
Penicillin G Sodium, IM, once

Prophylaxis: Penicillin G Sodium, IM, every 3-4 weeks

* for 5 years or up to 21 years old whichever is longer (if without carditis)
** for 10 years or up to 40 years old whichever is longer (if with carditis)

ANEURYSM

Problem: abnormal dilation of arterial segment  rupture  hemorrhage  shock  DEATH

Types
saccular – one segment of the artery
fusiform – entire segment of the artery
dissecting – tear in the intimal lining of the artery
Factors
Atherosclerosis #1
iNjuries to chest (chest trauma)
Effect of graft failure
Uncontrolled hypertension
aRteritis (associated with Kawasaki Disease)
In-borne / congenital (associated with Marfan’s Syndrome)
SLE (Systemic Lupus Erythematosus)
Male (40-70 years old and Caucasian)
Management
Duplex ultrasound  diagnostic test
Enough rest
Assess for rupture  “sudden and severe back pain”
Treat the underlying factor
Hypertension control
* Apresoline (Hydralazine)
* Sodium Nitroprusside (Nipride)
Surgery
* Aortic Resection
* Endovascular Graft (GoreTex)

Acute Respiratory Distress Syndrome (ARDS)

 “Non-cardiogenic Pulmonary Edema”
Factors:
* direct injury to lungs (aspiration, smoke inhalation)
* indirect insult to lungs (shock)
Problem:
sudden and progressive pulmonary edema

decreased lung compliance

impaired gas exchange

hypoxemia
S/Sx:
Arterial hypoxemia  “unresponsive to oxygen”
Retractions of chest  “intercostals retractions”
 aDventitious breath sound  “crackles”
Severe dyspnea  rapid onset (12-24 hours after an initiating event)
Management:
Assessment of respiratory status
 Arterial Blood Gas (ABG) #1
 Pulse Oximetry
 Pulmonary Function Test
Respiratory support
 Rest (to limit oxygen consumption)
 Oxygen therapy (to increase oxygenation supply)
 Mechanical ventilation (iron lung machine)
 Endotracheal intubation or tracheostomy ( to assist with mechanical ventilation)
Determine and treat the underlying condition
Supportive management
 Chest physiotherapy (CPT)
 Neuromuscular blocking agents  cause paralysis  assists with mechanical ventilation
* Pancuronium (Pavulon)
* Vecuronium (Norcuron)
 Neutrophil inhibitors
 Surfactant replacement therapy
 Corticosteroids (late stage)

DIVERTICULAR DISEASES
Cause: unknown
 Occurs most commonly in the sigmoid colon (Left Lower Quadrant)

Problem:
low fiber = small bulk of stool

increased intestinal peristalsis (an attempt to evacuate small bulk of stool)

increased intra-luminal pressure in the intestine

weakening of intestinal wall

dilation and outpouching of intestinal wall = “pouch”

(DIVERTICULUM = single outpouching)
(DIVERTICULOSIS = multiple outpouching)

entrapment of fecal matter in intestinal pouches

infection and inflammation of intestinal pouches

(DIVERTICULITIS)

perforation and rupture of intestinal pouches

infection and inflammation of peritoneum

(PERITONITIS)

S/Sx: Management:
Cramps Fluid intake is increased
Over-distention of abdomen Increase fiber intake and decrease fatty food
LLQ pain Bowel movement promotion
Over-flatulence * Psyllium (Metamucil)  bulk-forming laxative
N/V, anorexia * Docusate (Colace)  stool softener
Examine abdomen for possible complications (peritonitis)
Rx for pain
* Anti-cholinergic  reduces spasm
* Narcotic  pain reliever
Surgery
* Bowel resection
 IRRITABLE BOWEL SYNDROME (IBS)
Cause: unknown
Factors:
Stress (psychological)  depression and anxiety
Prevalence  more common among women than men
Alcohol and smoking
Stimulating and irritating food  spicy, fatty, caffeneited, beans
Mana  hereditary
Problem: “spastic” intestinal contractions / peristaltic waves  altered bowel pattern
S/Sx:
Altered bowel pattern #1
 diarrhea (due to increased intestinal motility) or
 constipation (due to intestinal spasm) or
 both diarrhea and constipation (alternating)
Abdominal pain (mild to severe)
Abdominal bloating
Abdominal distention

Management:
Pain management
 Propantheline Bromide (Pro-Banthine)  anti-cholinergic to decrease spasm
Altered bowel pattern management
 Loperamide (Imodium)  anti-diarrheal to decrease intestinal motility if with diarrhea
 Tegaserod (Zelnorm)  increases serotonin  to increase intestinal motility if with
constipation
Instructions to patient
 Reduce stress exposure
 Exercise (helps reduce stress and increases peristalsis if constipated)
 Chew food slowly and thoroughly
No smoking, alcohol and stimulating and irritating food (spicy, fatty, caffeneited, beans)
*** anti-depressant may be given if IBS is related to depression

ACUTE PANCREATITIS
Cause: Alcoholism
* increases production of pancreatic digestive enzymes especially Amylase
* causes spasm narrowing of pancreatic duct
Problem: Autodigestion (self-digestion)
* severe autodigestion can lead to hemorrhagic pancreatitis  internal bleeding
S/Sx:
Abdominal pain #1
Abdominal guarding
Anorexia, N/V
Management:
Pain management
* Morphine  narcotic  NEW DRUG OF CHOICE
 primary drug for acute and severe pain
* Meperidine  narcotic  OLD DRUG OF CHOICE
 breaks down into metabolites that can cross BBB  Seizure!
Anti-spasmodic
* Hyoscine (Buscopan)
NPO  during acute attack to prevent further production of pancreatic digestive enzyme
Check body areas with ecchymosis (bluish discoloration due to blood accumulation)
* peri-umbilical region  Cullen’s Sign HEMMORHAGIC PANCREATITIS
* flank region  Turner’s Sign
Rest  reduces production of pancreatic digestice enzymes
Endocrine disturbance
* Hyperglycemia  beta cells of Langerhans are also damaged during autodigestion
Administer prescribed medications
* Insulin  to reduce blood glucose level
* Cholecystokin (Pancreozymin)  relaxes the Sphincter of Oddi and pancreatic duct
Surgery  Whipple Surgery
Adrenal Gland
 “suprarenal” (above the kidneys)
 2 parts:
* adrenal medulla  produces catecholamines (epinephrine & norepinephrine)  sympathetic stiumulation
* adrenal cortex  produces cortisols (GMA)  corticosteroids of the body
* Glucocorticoid  Sugar  Glucose
* Mineralocorticoid  Salt  Na retention / K excretion
* Androgen  Sex  Sex hormone

CUSHINGS’s DISEASE ADDISON’s DISEASE

 “Hyperadrenocorticism”  “Adrenal Insuffiency”

 Problem: Hypersecretion of cortisols  Problem: Hyposecretion of cortisols

 Factors:  Factors:
* hyperplasia of adrenal gland * adrenalectomy
* tumor in the pituitary gland * abrupt withdrawal from steroid therapy
* steroid therapy * infection (Mycobacterium Tuberculosis)

 S/Sx:  S/Sx:
* Glucocorticoid * Glucocorticoid
 Sugar is high  Sugar is low
 Hyperglycemia  Hypoglycemia
 Hyperviscosity of blood  Hypoviscosity of blood
 Hypertension  Hypotension
 Delayed wound healing  Emaciation
 Central obesity  Severe weakness
* moon-face  Feeling of fatigue
* buffalo hump
* trunkal obesity
* thin limbs

* Mineralocorticoid *Mineralocorticoid
 Aldosterone is high  Aldosterone is low
 Hypernatremia  Hyponatremia
* Fluid retention = Edema * Fluid excretion = Dehydration = Shock
 Hypokalemia  Hyperkalemia
* Cardiac dysrhythmia * Cardiac dysrhythmia

* Androgen * Melanocyte Stimulating Hormone

 Sex Hormone  Melanin is high
 Among WOMEN  Hyperpigmentation = Eternal Tan (“bronze color”)
* hirsutism
* breast atrophy
* enlargement of clitoris
* amenorrhea

 Management: Management:
* Diet * Diet
 low carbohydrate  high carbohydrate
 low fluid  high fluid
 low sodium  moderate-high sodium
 high potassium  low potassium

* Drug: adrenal enzyme inhibitor * Drug: steroid therapy

 Mitotane  Prednisone, Hydrocortisone, Fludrocortisone
 Metyrapone * Detection of ADDISONIAN CRISIS
 Aminogluthetimide  triggered by stress, infection and exertion
 Ketoconazole  problem: circulatory shock

* Surgery
 Hypophysectomy (trans-sphenoidal)
 Adrenalectomy (unilateral / bilateral)
 management
* recumbent position with legs elevated
* IV fluid  D5NSS
* IV  Solu Cortef (steroid)
* Vasopressor  to increase BP
 PHEOCHROMOCYTOMA
 “10% Tumor”

 Adrenal Medulla Tumor (10% of cases are bilateral, malignant and originating from Chromaffin cells)
 Problem: oversecretion of cathecholamines (epinephrine and norepinephrine)
 S/Sx:  Dx:
“Sympathetic Over-stimulation” VMA Test (Vanilly Mandelic Acid)
Pressure elevation * 24-hour urine specimen
Pulse pressure widening
Pain  suboccipital region
Palpitaion  Management:
Pallor Pressure control  Phentolamine (Regitine)
Perspiration  Propanolol (Inderal)
Surgery  Adrenalectomy

SIADH DI
 Syndrome of Inappropriate ADH  Diabetes Insipidus
 Problem:  Problem:
Excessive ADH Lack of ADH

Oliguria  Fluid retention Polyuria  Diluted Urine

 USG (1.001-1.005)
Hypervolemia
Dehydration  Shock
Hypertension and Pulmonary Edema
Polydipsia
 Management:  Management:
Urine output monitoring Urine output and weight monitoring
Record the daily weight Replacement of fluid
Instruct to limit fluid intake IM injection  Vasopressin
Na restriction Nasal inhalation  Desmopressin
Emphasize drug compliance Encourage patient to wear medic alert
* ADH antagonist bracelet
 Demeclocycline
 Lithium
* Diuretics

Parathyroid Gland
 produces PTH ( parathormone / parathyrin / parathyroid hormone )
* increases serum calcium level
* promotes calcium release from the bones

HYPERPARATHYROIDISM
 Hypersecretion of PTH
* Primary Hyperparathyroidism  due to hyperfunction of parathyroid glands themselves
 related to hyperplasia, adenoma or carcinoma of the glands

* Secondary Hyperparthyroidism  due to physiological secretion of PTH in response to hypocalcemia

 related to vitamin D deficiency and chronic renal failure

 Problems:
* High PTH  Hypercalcemia (weakness, anorexia, N/V, polyuria, polydipsia, depression)
* Hypercalcemic crisis  Cognitive impairment  Coma
* Kidney Stones
 Calcium release from the bones
* Bone pain
* Fragile bones  Osteoporosis

 Management:
Fluid intake is increased  prevents stone formation
Risk for injury  fracture
* Priority: Safety
Avoid  alcohol, smoking, caffeinated and carbonated beverages (cause calcium loss from bones)
Good exercise to increase bone density
Instruct patient to report lethary (strong desire to sleep)  sign of Hypercalcemic Crisis
Lower the  serum calcium  give Cacitonin (decreases serum calcium level)
 PTH  give Cinacalcet (calcimimetic  mimics the effect of calcium  reduces PTH)
Ectomy (removal) of the parathyroid glands  Parathyroidectomy
 UTI (Urinay Tract Infection)
#1 nosocomial infection (hospital-acquired) due to improper catheterization technique
#1 causative agent: E coli (natural flora of intestine)
more common among women due to shorter urethra and proximity of anus and urethra

S/Sx Management
Pain
 dysuria Acidify the urine  cranberry juice
 suprapubic / flank pain Bubble bath  decreased acidity of vagina  AVOID!
Anorexia, N/V Cotton underpants
Increased Drug  “quinolones”  Ciprofloxacin (Ciprobay)
 WBC (Leukocytosis) Encourage fluid intake  at least 3L a day
 RBC in urine (Hematuria) Front to back wiping for women
 Temperature (Fever) Good personal hygiene
Note Health teaching  post-coital voiding (voiding after sex)
 CVA (costovertebral angle) tenderness
* indicator of pyelonephritis

CALCULI (“stones”)

terms types of stones

*urolithiasis: stone in the urinary tract acid stone
*ureterolithiasis: stone in the ureter *cystine: from protein-rich food (animal products like meat)
*nephrolithiasis: stone in the kidney *uric acid: from purine-rich food (organ meats, legumes)
alkaline stone
*calcium: from dairy products, calcium supplements
*oxalate: from tea, chocolate, green leafy vegetables
struvite
*infection: proteus, pseudomonas, klebsiella

S/Sx
Renal colic  severe flank pain
Elevated temperature  fever
Nausea & vomiting
Anorexia  loss of appetite
Leukocytosis  elevated WBC
Management
Strain the urine  use sterile gauze
 to collect a sample of stone
stone is sent to laboratory
Take plenty of fluid and encourage ambulation
Observe for hematuria (tea or cola-color urine)
Narcotic analgesic (Morphine) for pain
ESWL (extracorporeal shock wave lithotripsy)
Surgery  percutaneous nephrolithotomy

ACUTE RENAL FAILURE

sudden and almost complete loss of kidney function over a period of hours to days

categories
*pre-renal  due to impaired blood flow
 hemorrhage, heart failure, shock
*intra-renal  due to actual parenchymal damage to the glomeruli or kidney tubules
nephrotoxic drug (NSAID), hemolytic reaction
*post-renal  obstruction somewhere distal the kidney causing blockage to flow of urine
 calculi (stones)
phases
1.initiation period  begins with the initial insult and ends when oliguria develops
2.oliguria period  decreased urine output with elevation of urea, creatinine, and potassium in the blood
3.diuresis period  gradual increase in urine output, which signals that glomerular filtration has started to recover
4.recovery period  signals the improvement of renal function and may take 3 to 12 months

CHRONIC RENAL FAILURE

a progressive, irreversible deterioration in renal function

the body’s ability to maintain metabolic and fluid and electrolyte balance fails due to kidney function failure
result: uremia or azotemia (retention of urea and other nitrogenous wastes in the blood)
 ESRD (End Stage Renal Disease)  final stage
 < 10% is functional
 uremia or azotemia

Problems and Managements in ESRD

1.Anemia 5.Hypocalcemia
cause: low erythropoietin cause: inability to manufacture cholecalciferol
drug: recombinant human erythropoietin (EPOGEN) drug: calcium carbonate
IV/subQ 3x a week *** check hematocrit ***

6.Hyperphosphatemia
2.Pruritus (itchiness) calcium is inversely proportional to phosphate
cause: uremic frost (urea crystals deposited on the skin) drug: aluminum hydroxide
 diet: low protein

7.Hyperkalemia
3.Metabolic acidosis cause: inability to excrete excess serum potassium
cause: retention of acids risk: arrhythmia / cardiac arrest
drug: sodium bicarbonate management:

*low potassium diet

4.Fluid and sodium retention *avoid salt substitute (high in potassium)
cause: inability to excrete excess fluid *calcium gluconate (protects the heart)
management: *kayexalate (cation exchange resin)
*monitor weight and VS (hypertension) *sorbitol (laxative  diarrhea-effect  hypoK
*low fluid and sodium *glucose plus insulin (drives K to cell)
*anti-hypertensive *diuretic (K-wasting)
*DIALYSIS!!!

DIALYSIS

mechanical way of cleaning the blood

can be acute or chronic
processes involved in dialysis:
*diffusion – movement of toxins and wastes from an area of higher concentration (blood) to an area of lower concentration (dialysate)
*osmosis – movement of water from an area of higher solute concentration (blood) to an area of lower solute concentration (dialysate)
*ultrafiltration – movement of water from high pressure (blood) to an area of lower pressure (dialysate)
types:
*hemodialysis (most common)
*peritoneal dialysis

HEMODIALYSIS
done 3x a week, at least 3 – 4 hours per treatment
site of dialysis: DIALYZER (serves as a synthetic semipermeable membrane)
dialysate: a solution made up of all the important electrolytes in their ideal extracellular concentrations
vascular access: AV shunt or AV fistula (AV = arterio-venous)
*no BP and blood extraction on the affected arm
*check patency: bruit (auscultation) & thrill (palpation)
*prevent clotting: heparin (anticoagulant)
*prevent infection: aseptic technique
*danger!!! EXSANGUINATION (lethal blood loss) may occur if blood lines separate or dialysis needles accidentally dislodged
complications:
*psychological: reactive depression
*physiological: dialysis disequilibrium syndrome
cause: rapid dialysis rate causing cerebral fluid shift
S/Sx
*headache
*N/V
*restlessness
*decreasing LOC
*seizure
management: slow down / decrease the dialysis rate

PERITONEAL DIALYSIS
site of dialysis: PERITONEUM (serves as the semipermeable membrane)
sterile dialysate fluid is introduced into the peritoneal cavity through an abdominal catheter (Tenckhoff) made of silicone and are radiopaque to permit visualization through x-
ray

series of exchanges or cycles I peritoneal dialysis

1.infusion (2000 mL of dialysate to be administered in 5-10 minutes)
2.dwell (varies but peaks on the first 5 -10 minutes)
3.drainage (10 – 30 minutes)

entire exchange (infusion, dwell time, and drainage) takes 1 to 4 hours, depending on the prescribed dwell time
number of cycles or exchanges and their frequency are prescribed based on the patient’s physical status

monitor and compare input and output of fluid

*output = input  ok lang
*output > input  good
*output < input  bad (fluid is left inside)
 turn the patient from side to side
 elevate the head of bed

complications:
*peritonitis  most common
 # 1 staphylococcus aureus
 sign: cloudy drainage & abdominal pain
 antibiotic therapy for 10-14 days
*leakage  dialysate leaks through the incision
 prevented by using small volumes of dialysate (100-200 mL), gradually increasing to 2000 mL
*bleeding  common during the first few exchanges after a new catheter insertion
 stops in 1 to 2 days and requires no specific intervention
 may be observed occasionally, especially in young, menstruating women

KIDNEY TRANSPLANTATION

best donor: twin sign of kidney rejection

site of attachment of new kidney: iliac fossa *fever
immunosuppressants are given for life *weight gain
*purpose: to reduce the risk of rejection *hypertension
*risk: immunosuppression  infection *leukocytosis (elevated WBC)
*drugs: Cyclosporine, Prednisone, Imuran *pain on graft site