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Acute Kidney Injury pathophysiology
Is rapid reduction in kidney function resulting in failure to maintain waste elimination, fluid and electrolyte balance, and acid-base balance
occur over a few hours or days.
the most current definition of AKI is an increase in serum creatine by 0.3 mg/ dL ( 26.2 mcmil/L ) or more. Within 48 hrs
or an increase in serum creatine to 1.5 times or more from baseline
The glomerular filtration rate is accepted as the best overall indicator if it kind of functions, but it is not accurate during acute and critical illness.
AKI are reduced perfusion to the kidney, damage to kidney tissue, and obstruction of urine outflow
Urine outflow obstruction along with tissue damage of the kidneys and reduction of perfusion are causes of AKI
Twenty percent of all hospitalized patients and 60% of ICU patients develop AKI.
Complication with AKI
metabolic: Metabolic acidosis, hyperlipidemia, hyperkalemia, hyponatremia, hypocalcemia, hypophosphatemia
Cardiopulmonary
peripheral and pulmonary edema, heart failure, pulmonary embolism, pericarditis, pericardial effusion, hypertension, MI
Neurologic
Neuromuscular irritability or weakness, asteriixis, sexizure, mental status changes
Immune/infection
pneumonia and sepsis
Gastrointestinal
• N/V
• decreased peristalsis, enteral nutrition intolerance, malnutrition, ulcer formation, bleeding
Hematalogic
• bleeding, thrombosis, and anemia
Renal
• CKD, and end-stage kidney disease ( ESKD)
Labs & diagnosis
Elevated BUN & creatiene for AKI
• abnormal electrolyte value
• urine test
• dilute urine specific gravity greater than 1.030 and or near 1.000
• mayoglobin & hemoglobin may lead to nephron damage
• Ultrasonography: diagnosis kidney and indicate UTI, Kidney size,
• CT scans without contrast medium
• x-rays
• MAG3
• Kidney biopsy
• sodium may be normal, increased or decreased
• elevated,K+, phosphorus ,and blood osmolality
• Decreased Ca+, co2, HCO3, pco2 ( arterial blood), hemoglobin, hematocrit
• Mg+ , PH, increased or decreased
• Pelvis, KUB( abdominal x-ray)
Intervention & treatment for AKI
- treat underlying cause
• maintain normal fluid balance
• avoid drugs that alter kidney perfusion
• assess kidney before imaging test
• observe pt for new onset of edema
• weight daily
• assess I & O
• administer diuretic
• Monitor fluid and electrolyte replacement
• encourage diet low in K+, Mg+ and phosphorus
• avoid hypotension
• q4hrd
• renal diet low potassium, low phosphorusand high calcium
Indication of TURP
A surgical treatment for men with benign prostatic hyperplasia ( BPH) where a portion of the prostate is removed to improve urine flow or reduce urinary retention
patient are under anesthesia for the procedure
A small total is inserted through the urethraand excess prostate tissue is removed
patient typically stays inpatient for 1-2 days
TRUP: post op: continues bladder irrigation
prevent or remove blood clots after a surgical procedure
is common after TURP or blades surgery. Takes place over a day to several days in hospital setting
Complication of TURP
erectile dysfunction
• urinary continence
• UTI
• hematuria
• retrograde ejaculation
Managing continuous bladder irrigation
• ensure foley is placed using sterile techniques associated UTI
• adjust the rate of sterile fluid to prevent clots from forming.
• urine should be light pink
• ensure foley bag is emptied regularly
• maintain strict I & O.
Irrigation bags should be numbered to allow of the checking of irrigation fluid used
Continuous bladder irritation complication
- UTI
• Bladder perforation or tear
• pain
• bladder spasm
• bladder distention
• bladder trauma
UTI patho
A urinary tract infection is an infection in any part of the urinary tract
women are higher risk of developing urinary tract infection
S/S of UTI
• Urinary frequency
• Pain urination or burning
• fever
• color chnages in urine ( dark cloudy, or red in color
• odor
• tiredness
• N/V
• pain during sex
• pain in flank, abd, pelvic area or lower back
• cloudy, foul-smelling, and or dark pee`
• strong urge to tuinate but only passing a small amount urine
• pressure above the pubic bone
• confusion ( especially in older adults)
• lethargy ( especially in older adult
• back, side , or abdominal pain
Labs and diagnostic for UTI
urinalysis: urine check for cells such as WBC,germs such as bacteria or protein
•blood cults: urine checked for any bacterial growth found in the sample to determine the most appropriate antibiotic for treatment
•ultrasound, CT scan, cystoscopy: checks for damage, structural changes, obstructions/blockagesor tumor
Complication of UTI
urethritis : infection of the urethre
•pyelonephritis: kidney infection
- commonly caused by bacteria that travel up the urinay tract or a urinary obstruction blockage
•cystitis: bladder infection caused by bacteria moving up from the urethra
•Abscess: collection of pus anywhere along the urinary tract
Intervention/treatment of UTI
avoid unnecessary urinary catheterizations
• increase water intake
• do not hold in urine
• shower instead of tub bath
• wipe from front to back (women)
• women should avoid deodorants hygiene spraysand scented douches
• wear loos-fitting cotton underclothes
• clean genitalia before and after sex
• avoid coffee, spicy, and spicey food. Quit smoking
Most UTI must treated with therapy
• nitrofursntoin
• sulfanamides
• amoxicillin
• cephalosporin
• doxycycline
• fosfomycin
• quinolones
Patho of peritonotis
Peritoneal cavity normally contains 50 ml of sterile fluid
• which prevent friction in abdominal during peristalsis
• life threatening , acute inflammation and infection of visceral/parietal peritoneum and endothelial lining of abdominal activity
• when cavity is contaminated by bacteria, the body begin an inflammatory reaction walling of a localized area to fight the infection
Risk factor for peritonitis
bacteria such as escherichia coli, streptococcus, staphylococcus, pneumococci, and gonococci
• chemical peritonitis
• young adults with with appendicitis
• older adults with decreased immunity
Sign and symptom of peritonits
rigid birdlike abdomen ( classic)
• abdominal pain ( localized, poorly localized or referred to the shoulder or chest)
• listened abdomen
• N/V
• anorexia
• diminished bowel sound
• inability to pass flats or feces
• rebound tenderness in the abdomen
• high fever
• tachycardi a
• dehydration from high fever ( poor skin turgor)
• decreased urine output
• hiccups
• possible compromise in respiratory status
• laying with knee flexed or still
• cardinal signs: abdominal pain, tenderness, and distention
• with generalized tenderness is wide spread and with localized tender abdomen
what is the goal for pt with peritonitis ?
relief or control pain and fluid and electrolyte balance
Intervention for peritonitis
observe for tenderness abdomen with rebound tenderness on palpation
• usually non surgical
• but surgery may be perform to remove abscess
• assess vital signs frequent for any changes for septic ( unresolved or progressive hypotension, decreased pulse pressure, tachycardia fever, skin changes or tachypnea
• monitor mental status
• administer antibiotics as prescribed
• provide oxygen
• abdominal surgery may be prescribed to help determine cause and report
• Hypertonic IV fluids daily weights with same cloth, same scale and same time
• record I&0
• restore fluid and electrolyte
• NPO
• NGT suctioning
• monitor patient for fluid retention
• educate pt for s/s of infection
patho for appedicitis
extend off the proximal cecum of the colon just below ileocecal valve
• inflammation occur when the lumen ( opening) of the appendix is obstructed ( blocked) leading to infection as bacteria invade the wall of appendix
• usually result form very hard feces
• when lumen is blocked, the mucosa secretes fluid increasing the internal pressure and restricting blood flow , which causes pain.
• abscess may develop if process occurs slowly
• rapid process may resulting peritonitis
complication of appendicitis
peritonitis, gangrene, sepsis, perforation can occur
S/S of appendicitis
right lower quadrant ( RLQ)
• abdominal pain followed by N/V
• cramping pain in the epigastric or periumbilical area
• anorexia
• pain can be anywhere in the abdomen or flank area
• pain in RLQ between anterior iliac breast to umbilicus = infection progression (Mcburney point)
• rebound tenderness
Labs for appendicitis
WBC greater 20,000 ( perforated appendix )
• leuckocyotsis 10,00 to 18,00
• CT: presence of fecaloma ( small stone or feces)
Appendicitis inetrvention
• keep patient on NPO
• remain semifowler position are tolerated
• pt should not receive laxative or exams can cause perforation
• no heat to the abdomen (may increase circulation to the appendix result in inflammation and perforation)
• pt with suspected appendicitis administer IV fluid and pain fluid and electrolyte balance
• Most patient require surgery
Surgery
• appendectomy
• Laparoscopy
PUD patho
result when GI mucosal defense becomes impaired and no longer protect mucosal defense become impaired and no longer protect the epithelium from the effects of acid and pepsin
• Mainly caused by H. Pylori infection
• oral to oral ( stomach transmitted from mouth to mouth or fecal to oral ( from stool to mouth) contact
• As a response to the bacteria, cytokines, neutrophils, and other substances are activated and cause epithelial cell necrosis
Risk factor of PUD
H.pylori
• long-term use of Nsaid, such as ibuprofen
• Zollinger Ellison syndrome ( neuro endocrine tumor)
Types of PUD ulcers
duodenal ulcers
• occur more often than other types
• pressent in upper portion of the duodenum
• deep sharply demarcated lesion that penetrates through mucosa and submucosa into muscularis propria
• floor ulcer is necrotic
• high gastric acid and acid secretion
• low PH (excess acid)
• develop in the antrum of the stomach
• commonly caused by H pylor
Stress
• acute
• mucosal lesions occurring after acute medical crisis or trauma, sepsis or head injury
• may lead to gastric ulcer if pt is NPO for major surgery
• biggest thing is bleeding caused by gastric erosion can lead to mass hemorrhage
duodenal ulcers
• occur more often than other types
• pressent in upper portion of the duodenum
• deep sharply demarcated lesion that penetrates through music and submucosa into muscularis propria
• floor ulcer is necrotic
• high gastric acid and acid secretion
• low PH ( excess acid)
• evelop in the antrum of the stomach
• commonly caused by H pylor
Stress
• acute
• mucosal lesions occurring after acute medical crisis or trauma scubas sepsis or head injury
• may lead to gastric ulcer if pt nPO for major surgery
• biggest thing is bleeding caused by gastric erosion can lead to mass hemorrhage
S/S of PUD
Sign & symptom
• bight red or coffee ground vomitus (hematemesis)
• melena (tarry or dark sticky stools)
• decreased hemoglobin and hematocrit
• decreased blood pressure
• increased HR
• weak peripheral pulses
• acute confusion ( in older adults)
• vertigo
• dizziness or lightheadedness
• syncope (loss of consciousness)
• epigastric tenderness and pain (located in umbilicus and diploid processes)
• rigid, boardlike abdomen with rebound tenderness if perforation into the perineal cavity
• hyperactive bowel sound on auscultation diminished with progression
• dyspepsia: pt may report sharp, burningor gnawing pain
PUD complucations
- hemorrhage, perforation pyloric obstruction and intractable disease
• hemorrhage is the most serious complication.
• if underlying H.pylori stays untreated second episode of bleeding may occur if therapy does not include an H2 antagonist or PPI
PUD labs & diagnostic
blod
• breath
• stool
• serologic testing for H pylori antibodies ( most common
• urea breath test: swallowing a capsule, liquid, or pudding that contains radioactive carbon urea (13C urea). After a few minutes the patient exhales; if the radioactive carbon is found, the bacterium is present
• stool antigen test
• decreased H&H
• positive occult
• esophagogastroduodenoscopy ( most accurate test)
• rapid urease test
• medicine scan: injected with contrast media
PUD: intervention
avoid any food that may cause discomfort
• encourage a bland, nonirritating diet
• avoif bed time snacks during symptomatic phas
• avoid alcohol and tobacco
• avoid caffeine
• complementary
• fluid and blood ( due to vomiting nag bleeding )
• monitor fluid status
• I & O
• fluid replacement should be monitor especially in older adults to avoid fluid overload
• open surgery : pt down 4-6 weeks
• avoid spicy food, alcohol, tobacco
• ensure food digest before laying down
• educate change of position
• Ng tube to help empty gastric content
• small frequent meal
• educate share, sudden, persistent and severe gastric or abdominal pain, blood or black stools, blood, vomit or vomit that look like coffee grounds contact HCP.
• nonsurgical : active bleeding is life threatening emergency
surgical
• minimally invasive and conventional open surgery
• minimally invasive: remove a chronic gastric ulcer or treat hemorrhage from perforation
avoid any food that may cause discomfort
• encourage a bland, nonirritating diet
• avoif bed time snacks during symptomatic phas
• avoid alcohol and tobacco
• avoid caffeine
• complementary
• fluid and blood ( due to vomiting nag bleeding )
• monitor fluid status
• I & O
• fluid replacement should be monitor especially in older adults to avoid fluid overload
• open surgery : pt down 4-6 weeks
• avoid spicy food, alcohol, tobacco
• ensure food digest before laying down
• educate change of position
• Ng tube to help empty gastric content
• small frequent meal
• educate share, sudden, persistent and severe gastric or abdominal pain, blood or black stools, blood, vomit or vomit that look like coffee grounds contact HCP.
• nonsurgical : active bleeding is life threatening emergency
surgical
• minimally invasive and conventional open surgery
• minimally invasive: remove a chronic gastric ulcer or treat hemorrhage from perforation
PUD: drugs
PPIs
“Prazole”
• omeprazole
• do not discontinue suddenly
• encourage anyone with PUD to avoid aspirin
• they can
• use bismuth with caution
• can take anti biotic
Acute pancreatitis: patho
serious and life-threatening inflammation of the pancreas
• Caused by a premature activation of excessive pancreatic enyzme that destroy ductal tissue and pancreatic cells, leading to digestion and fibrosis of the pancreas
• severity depend on extent of inflammation and tissue damage
• rang from mild, which pt may have dema and inflammation, to necrotizing hemorrhagic pancreatitis
Acute pancreatitis: complication
• Jaundice
• hyperglycemia
• DM
• left lung pleural effusion
• atelectasis
• pneumonia
• multisystem organ failure
• acute respiratory distress syndrome ( pulmonary edema0)
• pulmonary failure
• acute kidney failure
• coagulation defect
• DIC
• Shock leading to peripheral vasodilation
• hypovolemia
Acute pancreatitis: S/S
serve abdominal pain in mid epigastric area or left upper quadrant
• pain radiate to the back left flank or shoulder
• pain described as tense, boring feeling that is going through the body
• worsens by lying in supine position
• relief by assuming in the fetal position with none drawn up to the chest and spine flexed or by siting upright and bending forward
• weight loss resulting in N/V
Acute pancreatitis
pain due to inflammation ,weight loss and inadequate nutrition due to inability to digest food and absorb nutrient
Acute pancreatitis: labs & diagnostic
elevated amylase
• elevated lipase
• elevated trypsin
• elevated elastase
• elevated glucose
• decrease Ca+ and Mg+
• elevated bilirubin
• elevated ALT
• elevated AST
• elevated WBC & ESR
• abdominal ultrasound
• Ct scan
• x-ray reveal gallstones
• chest X-ray may show pleural effusion
• ERCP diagnosed pancreatitis stones
Acute pancreatitis: intervention
• offer support
• assess ABC
• provide oxygen PRN
• Control pain, “ severe boring abd pain” is common
• hydration with IV fluid
• fasting and rest
• monitor for hemodynamic
• NPO during acute period
• measure I &O
• suctioning for pt who are ill with N/V
• Assess frequently for the return of peristalsis by asking patients
• help pt with side lying position ( fetal position)
• frequent oral and nares hygiene for pt who have NGT
• monitor respiration every 4 hrs
• assess weight gain for fluid overload
• observe for dyspnea
• observe fro hypocalmeia (muscle twitching, numbness and irritability)
• surgical intervention not indicated
• enteral feeding is preferred over total parenteral nutrition (TPN) because it causes fewer episodes of glucose elevation & other associated complications
• small frequent moderate to high carb
• high protein, low fat meals
• bland food with little spice
• avoid GI stimulants such as coffee , tea, cola , chocolate and alcohol
• soluble and vitmains and mineral replacement
• limit stirs climbingand other strenuous activity until regain strength
insulin
antimemetics
opooids
Acute pancreatitis: other findings
Generalized jaundice
• Gray-blue discoloration of the abdomen and periumbilical area
• Gray-blue discoloration of the flanks, caused by pancreatic enzyme leakage to cutaneous tissue from the peritoneal cavity
Diabetes Insipidus: patho
-Known as arginine vasopressin deficiency
• disorder of the posterior pituitary gland in which water is caused by a deficiency in vasopressin ( antidiuretic hormone ADH)
• or inability of the kidney to respond to vasopressin is the resistance the arginine vasopressin
• excretion of large volume of urine that is going to be diluted because the kidney do not reabsorb water
• Massive water loss increases plasma osmolarity and serum sodium levels, which stimulate the sensation of thirst.
• Thirst promotes increased fluid intake and aids in maintaining hydration.
• leads to polyuria, dehydration leading to electrolyte imbalance
• ADH tell our body to hold on to all the fluid
*
DI: Risk factor
Surgery
• head trauma
• drug use ( lithium)
DI: sign and symptom
polyuria
• nocturia ( increased urination)
• polydipsia
• dehydration
• poor skin tugor
• dry or cracked mucus memberane
• urine output more than 3 L greater than volume ingested
DI: preventative measure
Ensure that no pt suspected of having DI is deprived of fluid for more than 4 hours because these pt cannot reduce urine output and severe dehydration can result
DI: intervention & treatment
24 intake monitor intake, include all IV pushes and drips,
• offer fluid minimum fluid and what they are taking in is matching the output
• patient can lose 4- 30 L day of urine
• educate to weight everyday
• pee before weight
• wear medical alert bracelet
• weight gain more than 2.2 lb along with other signs of water toxicity ( persistent headache, acute confusion, nausea, vomiting), instruct the patient to go immediately to the ED)
• limit intake of Na+ protein and diuretics
• sodium less tan 2.3
• drink fluid equal amount of urine output
• educate pt polyuria, polydipsia indicate need for another dose.
DI: drugs
desmopressin
• replace natural vasopressin ( ADH)
• chest tightness, allergy, and lung inhalation.
• can cause fluid overload
• if pt have respiratory infection or side effect we they can admin subq or oral
• educate pt to weight self daily with same scale and clot.
Syndrome of inappropriate antidiuretic Hormone (SIADH) : Patho
• known as Schwartz-Bartter syndrome
• a problem in which ADH is secreted even when plasma osmolarity is low or normal
• resulting in water retention and fluid overload
• A decrease in plasma osmolarity normally inhibits ADH production and secretion.
• vessel pressure continues to be released even when not needed, leading to water retention and overload.
• can occur with cancer therapy, pulmonary infection impaired
• ADH continues to be released when not needed, leading to water retention and disturbances of fluid and electrolyte balance
leads to hyponatremia , and fluid overload
SIADH: risk factor/ cause
small cell lung cancer
• pancreatic duodenal and GU carcinomas
• thymoma
• Hodgkin lymphoma
• tauma
• infection
• tumor
• visual and bacterial pneumonia
• lung abscesses
• SSRis, MAOIs
SIADH: S/S
hyponatremia
• loss of appetite
• N/V
• weight gain ( no dependent edema because only water retained not salt
• ependent edema is not present but a puffiness because it not sodium
• fluid shift which affect CNS function
• patient may start to develop confusion , altered mental status , disorientation, hostile , lethargy decrease responsiveness, seizuure, coma
• - decreased deep tendon reflex
• bounding pulses
• hypothermic
• decrease urine volume but increase osmolarity that means the concentration of urine
• meaning sign of hyponatremia
• headache
• lethargy
• hostility
• disorientation and changes In LOC
• decreased DTR
• bounding pulses due to fluid overload
• hypothermia may be present due to CNS disturbance)
SIADH: intervention
• assess pt for headache and lethergy can lead to decrease responsiveness, seizures and come
• assess DTR
• educate pt and family about fluid restriction and medication adherence and injury
• fluid may be restricted to 500 to 100/ 24hrs
• depending on patient
• daily weight
• hypotonic solution ( hponatremia in base line)
• listen to respiratory status
• be cautious with pushing saline we do not want extra fluid in their system
• encourage small sip
• ice chips
• mouth swab do not swallow the water from mouth swab.
• if they gain 2.2
SIADH: drugs
Vaptans
• can increase Na+
• monitor pt for pulmonary edema
• bounding pulses ( lower intake)
• JVD
Adrenal Gland Hypofunction ( : patho
Adrenal Gland Hypofunction, also known as Addison's disease, occurs when the adrenal glands produce insufficient amounts of cortisol and aldosterone. This results in various metabolic dysregulations, including decreased stress response, electrolyte imbalances, and increased pigmentation of the skin.
• Production of steroids hormone may decrease as result of inadequate secretion of adrenocorticotropic hormone ( ACTH) , dysfunction of the hypothalamic-pituitary control mechanism, or direct problems of adrenal gland tissue
gradully or can occur quickly with stress
• causes problems through the loss of aldosterone and cortisol action
• Decreased cortisol levels result in hypoglycemia
• Gastric acid production and glomerular filtration decrease
• leads to decrease in BUN—> anorexia and weight loss
• reduce in aldosterone secretion causes fluid and electrolyte balance
• K+ is decrease
• Na+ & water secretion increases —> hyponatremia and hypovolemia
• Potassium retention also promotes reabsorption of hydrogen ions, which can lead to acidosis.
Acute adrenal insufficiency
• adrenal crisis or Addison crisis
• medical emergency
• need for cortisol and aldosterone is greater than the body supply
• life threatening symptom without warning
• occur due stressful even such as surgery, trauma, severe infection, especially when adrenal hormone output is reduced
• sodium falls and K+ rises rapidly
Adrenal Glend Hypofunction: primary & secondary
Primary: glucocorticoids, mineralcorticoids, and androgen are reduced
Secondary:
• mineralocorticoid function is preserved; sudden cessation go long-term glucocorticoid therapy (common)
• crisis from long-term use and abruptly stoppin
Adrenal Gland Hypofunction: S/S
anemia
• hypercalcemia
• hyponatremia
• hypotension
• abdominal pain
• anorexia
• constipation or diarrhea
• N/V
• salt craving
• weight loss
• hyperpigmentation
• vitiligo
• fatigue
• joint pain
• muscle pain
• muscle wekaness
• Hair may decrease
• hypoglycemia ( sweating, headaches, tachycardia, tremors)
• fluid depletion ( postural hypotension and dehydration)
• hyponatremia ( hypotension and decrease cognition )
ADH: labs and diagnostic
Diagnsotic
• CT & MRI
• low Na+ leve
• Low salivary cortisol level
• elevated BUN & K+
• ACTH stimulation test (given IV): plasma cortisol levels are obtained at 30-minute and 1-hour intervals.
ADH: Psychosocial
pt may appear lethargic, depressed confused and even psychotic
• pt family may report pt has wide mood swing
• Intervention: Assess the patient’s orientation to person, place, time, and situation.
ADH: intervention & treatment
prevent hypoglycemia
• fluid balance
• assess pt for K+
• assess vital every 1-4 hours depending on pt condition and presence of dysrhythmias or postural hypotension
• weight pt daily
• record I &O
• monitor lab values
• fluid replacement help with cortisol and aldosterone deficiencies
ADH: drugs
Cortisol and aldosterone deficiencies are corrected by hormone replacement therapy
• Hydrocortisone corrects glucocorticoid deficiency
• Oral cortisol replacement regimens and dosages vary.
• most common drug is prednisone
• prednisolone is more potent that is the only difference.
• fludrotisone may be needed to maintain to restore fluid and electrolyte balance ( especially sodium and potassium))
• prednisone 2/3 if given in the morning and the rest is given in the evening.
• adjust medication based ob theater
Cushing Syndrome: patho
A hormonal disorder caused by prolonged exposure to high levels of cortisol, often due to a tumor or excess production by the adrenal glands. Symptoms include weight gain, rounded face, and high blood pressure.
hypercortisolism
• Excessive tissue exposure to cortisol and other glucocorticoids ( cushing syndrome)
• An increase in total body fat results from slow turnover of plasma fatty acids
Cushing syndorme: Risk factor
prendnisone
• benign hormone secreting tumor
• pituitary hyperplasia
Cushing syndrome: S/S
• truncated obesity
• buffalo hump
• moon face
• muscle
• bone density loss
• hypoglycemia
• pale skin
• GI distance
• weakness
• changes in distribution of body hair
• bronze pigmentation of skin
• postural hypotension
• petechie muscle atrophy
• thin skin and fragile capillaries
• hairy (hirsutism)
• acne
• infrequent menses ( oligomenorrhea)
• disrupt ovarian hormone
• hypertension
• brusing
• petechie
• frequent depends edema
• osteoporosis
• muscle atrophy
• increased infection
cushing syndrome: priority
1.Fluid overload due to hormone-induced water and sodium retention
2. Potential for injury due to skin thinning, poor wound healing, and bone density loss
3. Potential for infection due to hormone-induced reduced immunity
Cushing syndrome: Labs & diagnostic
blood: detect hypercortisolism
• salivary
• urine cortisol levels: collect 24hrs specimen
• ACTH level eleavted
• if cause is steroid is low
• dexamethasone:
• drawn at bed time, fasting blood draw us performed the next morning at 8 a.m to assess plasma cortisol level followed by other urine test
• when cortisol level are suppressed by dexamethasone cushing disease is not present
• increase glucose level
• decrease lymphocyte count
• increase sodium
• decreased serum calcium level
Cushing syndrome: intervention & treatment
• fluid and electrolyte balance
• cortisol
Treatment
• depending on type of cushion
• Address the cause
• monitor fluid overload
• `use pressure-reducing or pressure-relieving overlay on the mattress
• assess skin pressure areas
• especially coccyx, elbows, hips, heels daily redness, hyperpigmentation, or open areas
• if pt has nasal cannula check skin
• help change position every 2 hours
Cushing sryndorme drugs
• Ketoconazole and levoketoconazole
• Ketoconazole can cause reversible liver damage, so liver function tests must be closely followed
Hyperglycemic-hyperosmolar state (HHS): patho
A serious condition characterized by extremely high blood glucose levels and increased serum osmolality, often resulting from insulin deficiency and dehydration. It commonly occurs in individuals with diabetes, particularly type 2, and can lead to severe electrolyte imbalances and altered mental status.
is increased blood osmolarity
• caused by hyperglycemia
• result from sustain osmotic diuresis leading extremely high glucose levels
• caused by hyperglycemia and dehydration
• no ketone present or low
• BG level may exceed 600 or more
• blood osmolarity may exceed 320 most/ L
• gradual on set
• Most common in type 2
• medical emergency
• body secrete insulin to prevent ketone but not enough for
HHS: Risk factors
• steroid
• diuretics
• dehydration
• infection
• severe insulin resistance and dehydration
• pancreatitis
• storke, MI, trauma
HHS: Complication
• seizure and coma ( the biggy)
• shock and multi organ failure
• cerebral edema ( rare but life threatening)
• thromboembolism ( DVT, stroke, MI) due to dehydration)
• acute kidney injury due to severe dehydration
HHS: S/S
severe hyperglycemia >600
• dehydration ( dry skin, sunken eyes, poor, skin
• altered mental status ( confusion, lethargy, seizures, coma)
• neurological deficit ( weakness, speech disturbance, altered mental status, lethergy, seizure and coma)
• polyuria and polydipsia ( early)
• hypotension & tachycardia ( due to dehydration
• coma occur when blood osmarlity is greater than 350 270-300)
• reversible poresis
• monitor for both hypo and hyperhalemia
• hyponatremia ( LOC , mental staus charges)
• Hypokalemia
HHS: Intervention and Treatment
• monito hypoand hyperkalemia
• assess vs
• monitor neurologic staus
• monitor eyes and nose
• assess for infection
• monitor lab for WBC
• monitor electrolyte imbalance
• monitor for fluid overload
• normal saline first and hypotonic for fluid replacement
• Iv potassium: monitor for cardiac dysrhythmias
• insulin therapy: low dose IV insulin infusion ( careful to avoid rapid shifts) and monitor glucose level
• monitor and treat underlying causes: antibiotic for infection and address medication induced hyperglycemia
• Prevent complication: frequent neurological check for cerebral edema and monitor for hypoglycemia and EI
• stay hydrated
• medication adherence
• educate pt early and late sign of hypoglycemia
• frequency blood sugar check
• follow six day rules
• manage infection promptly
when is blood glucose retsore in pt with HHS?
36-72 hrs! To rehydrate and get BS under control
Diabetic ketoacidosis (DKA) :
a serious diabetes complication characterized by high blood sugar levels, ketones in the urine, and acidosis. It occurs when the body doesn't have enough insulin and begins to break down fat for energy.
• complication of diabetes characterized by hypoglycemia, metabolic aacidosisnd increased production of ketones
• caused by abscence of insulin and generation of ketones,
• uncontrolled hyperglycemia, metabolic acidosisand increased production of ketone
• result from combination of insulin defacing and body metabolizing triglyceride and amino acids glucose instead for energy and increase in hormone
• rapid onset
• a lot of gastrointestinal system
• serum glucose more than 300
• medical emergency!
DKA: Risk factor
• infection illness
• gastroporesis
• steroids
• diuretics
DKA: complication
cerebral edema
• heart failure
• Pulmonary edema
• hypokalemia ( cause you correct glucose level)
• hypoglycemia
• coma
• kidney failure
• death
• before giving potassium ensure urine output Is 30 ml.
DKA: S/S
• polyuria
• polydipsia
polyphagia
• fruity odor breath
• vomiting
• abdominal pain, N/V
• weakness
• lethergy
• comfusion
Kyperkalemia
• Kussmaul respiration—> shock and coma with increased ketone
DKA: Labs & diagnostic
Blood glucose levels over 250 mg/dL, elevated ketones in urine and blood, metabolic acidosis with low bicarbonate levels, and anion gap acidosis.
• blood glucose > 250
• positive ketones in blood urine
• ABG (PH <7.3,HCO3 < 18 mEg/L
DKA: intervention & treatment
• airways is first! Followed by LOC, hydration ,electrolytes, blood glucose level and VS
• level of consciousness , hydration status electrolyte and blood glucose level
• check pt BP, pulse, respiratory q15 mins
• drink 3L a day and increase if they become ill
• check vitals every 15 mins
• record I&O, temp. And mental status every hour
• assess central venous pressure every 30 mins if central venous catheter present.
• after pt is stable assess vitals q4
• assess weight loss, skin tumor, thirst, dry mucus membrane and oliguria with high specific gravity
• assess for wean and rapid pulses
• flat neck viens, increased temperature
• check glucose
• check ketone
• stay hydrated
• follow carb diet.( 150 gram)
Treatment
• normal saline fluid initially ( isotonic )
• IV dextrose in 0.45% ( hypotonic)
• insulin gtt
• bicarb
• 2L fluid everyday and increase if ill
When is DKA resolved?
oral insulin resolved when glucose less than 200 HCO3 greater than 18, and PH is 7.3.
PUD: priority
• acute or persistent pain due to gastric/duodenal ulceration
• potential for upper GI bleeding due to gastric and/or duodenal ulceration perforation
• Goal: pain control of 3 or less
Goal
• Does not have active PUD or H. pylori infection
• Verbalizes relief or control of pain
• Adheres to the drug regimen and lifestyle changes to prevent recurrence and heal the ulcer
• Does not experience upper GI bleeding; if bleeding occurs, it will be promptly and effectively managed.
Sick-Day Rules
• Notify your primary healthcare provider or diabetes health care provider that you are ill.
• Monitor your blood glucose at least every 2 to 4 hours.
• Test your urine for ketones even if your blood glucose is in range, particularly if you are vomiting.
• Continue to take insulin or other antidiabetic agents unless instructed otherwise by your diabetes health care provider.
• To prevent dehydration, drink 8 to 12 ounces (240–360 mL) of sugar-free liquids every hour that you are awake. If your blood glucose level is below your target range, drink fluids that contain sugar.
• Continue to eat meals at regular times.
• If unable to tolerate solid food because of nausea, consume more easily tolerated foods or liquids equal to the carbohydrate content of your usual meal.
• Call your diabetes health care provider for any of these problems:
• Persistent nausea and vomiting
• Persistent hypoglycemia
• Moderate or high ketones
• Blood glucose elevation after two supplemental doses of insulin
• High (101.5°F [38.6°C]) temperature or increasing fever; fever for more than 24 hours
• Treat diarrhea, nausea, vomiting, and fever as directed by your diabetes health care provider.
• Get plenty of rest.
Foot Care Instructions
Inspect your feet daily, especially the area between the toes.
• Wash your feet daily with lukewarm water and soap. Dry thoroughly.
• Apply a moisturizer to your feet (but not between your toes) after bathing.
• Change into clean cotton socks every day.
• Do not wear the same pair of shoes 2 days in a row, and wear only shoes made of breathable materials, such as leather or cloth.
• Check your shoes for foreign objects (pebbles) before putting them on. Check inside the shoes for cracks or tears in the lining.
• Buy shoes that have plenty of room for your toes. Buy shoes later in the day when feet are normally larger. Break in new shoes gradually.
• Wear socks to keep your feet warm.
• Trim your nails straight across with a nail clipper and smooth them with an emery board.
• See your diabetes health care provider immediately if you have blisters, sores, or infections. Protect the area with a dry, sterile dressing. Do not use tape to secure dressing to the skin.
• Do not treat blisters, sores, or infections with home remedies.
• Do not step into the bathtub without checking the temperature of the water with your wrist or thermometer.
• Do not use very hot or cold water. Never use hot-water bottles, heating pads, or portable heaters to warm your feet.
• Do not treat corns, blisters, bunions, calluses, or ingrown toenails yourself.
• Do not go barefooted.
• Do not wear sandals with open toes or straps between the toes.
• Do not cross your legs or wear tight stockings that constrict blood flow.
DM: diabetes
chronic condition in which the ability to produce or use the hormone insulin is impaired
• resulting in impaired glucose metabolism and can affect function of all body systems
• the pancreas regulate digestion through its exocrine function and endure glucose regulation through it’s endocrine functions
• endocrine pancreas has about 1 million small glands, the islet of langerhans scattered through the organs
• inside the islet are two types of cells important to glucose regulationthese are alpha and beta cells
• Alpha secretes glucagonand beta produce insulin and amylin
type 1
• beta cell destruction leading to absolute insulin deficiency
• autoimmune
• when pt doesn’t have any insulin
• beta cell of the langerhans have been destroyed
• can happen to young children
• certain infection, such as coxsackievirus
Type 2
• doesn’t respond to insulin
• the glucose hang in the body
DM: Risk factor
Risk factor
• smoking
• physcoa; inactivity
• obesity
• hypertension
• hyperlipidemia
• metabolic syndrome
DM: S/S
polyuira
polydipsia
polyphagia
extreme fatigue
blurred vision
slow-healing sores
unintended weight loss.
headache
DM: Labs & diagnsotic
glucose level
glycosylated hemoglobin (A1c)
• previous 3 months and indicate average glucose level
• shows average BS level during the previous 120 days
fasting glucose:
• use to diagnose DM in nonpregnant pt
Oral glucose tolerance
• used for gestational diabetes
Screening for diabetes
• Detect predates and T2DM
continuing glucose monitoring
• on gong time period oe for short assessment time 7- 14 days
• inserted underneath pt skin to measure glucose in continuing basis
DM: intervention
• weight loss
• physical activity
• balanced diet
• lowering triglyceride level , increasing HDL
• smoking cessation
• keep BS level within normal range
• follow up with HCP to have eye and vision checked
• urine albumin level checked yearly
• encourage daily foot inspections
• Assess symptom of hypo and hyperglycemia
• assess hypoglycemic unawareness
• assess before and after exercise
• assess gastropporeiss
• eat at least 25g of fiber daily
• avoid sure sweetened beveragesincluding high fructose corn syrup
• limit alcohol use. 2 for male and 1 for female .
Hyperglycemia
• Fatigue
• flushed skin
• frequent urination
• dry mouth, excessive thirst
• rapid bretahing
• fruity odor breathing (kussumaul respiration)
• drowisness
• headache
• decreased reflexes
Hypoglycemia
• shakeiness (tremors)
• sweating
• pallor
• cool skin
• disorientation
• headache
• hunger
• blurred vision
• can lead to seizure and death
Gastritis: patho
inflammation of the stomach lining, which can be caused by factors such as infection, long-term use of NSAIDs, excessive alcohol use, or autoimmune disorders leading to gastric mucosal damage.
can be erosive (causing ulcers) or nonerosive.
worsen with histamine release and vagal stimulation
chronic: apthcy, diffuse (spread out) imflammation of the mucosal lining of the stomach and atrophy
most common form of chronic is caused by H.pylori
Acute gastritis is treated symptomatically and supportively because the healing process is spontaneous, usually occurring within a few days.
Gastritis: S/S
rapid onset of epigastric pain
dyspepsia ( “ epigastric burning sensation or heartburn”
bleeding may occur or metaemesis
melena “ dark tarry stool”
stomach pain
N/V
Gatritis : Intervention and treatment
eat well-balanced diet
exercise regulary
avoid drinking excessive amounts of alcohol
avoid long-term use of coffee
consume food free of contamination
manage stress level by using complementary therapy
stop smoking
get help if experiencing GERD
Protect yourself against exposures such as lead and nickel
Metallic syndrome
• abdominal obesity: waist 40 inch or more for men and 35 inches or more for women
• hyperglycemia: fasting glucose level of 100
• hypertension: systolic of blood pressure 140 or diastolic BP of 90 or more
• hyperlipidemia : triglyceride level of 150 ombre, Hal less than 40 for men and 50 for women