Patho Exam 2 Flashcards
sickle cell anemia
Cluster of autosomal recessive disorders
- hemoglobin sickle or crescent in shape
- genetic mutation
Pathogenesis
- hemoglobin cannot bind oxygen effectively
- RBC collapses into sickle shape when oxygen released
- RBC clump together and obstruct blood flow
- RBC lifespan 10-20 days (as compared to 120 days)
- chronic inflammation
sickle cell disease is caused by an inherited autosomal recessive defect in hemoglobin synthesis
sickle cell disease is characterized by episodes of acute painful crises that are triggered by conditions that cause high oxygen demand
clinical manifestations
- hypoxia
- tissue ischemia
treatment:
- prevention, screening
- supportive care
- disease-modifying strategies
- curative procedures
- genetic analysis, prenatal counseling
- HYDROXYUREMA DRUG USED
sickle cell crisis
blood coagulates in the spleen, the eyes could also be affected
**this individual should maintain high volume, drink lots of fluids
Thalassemia
Group of autosomal recessive diseases that affect production of hemoglobin
- increased incidence in individuals from Mediterranean and Asia
Cause
- defect in production of one or more globin chains
clinical manifestations
- defects at birth (growth retardation and cognitive deficits)
- jaundice
aplastic anemia
decrease in all cell populations produced by bone marrow
- erythrocytes, leukocytes, platelets
- body stops producing enough new blood cells
causes:
- genetic
- viral exposure
-drugs or toxins
-immune-mediated attack on bone marrow
diagnosis:
- decreased white blood cells, platelets, RBCs, reduced hemoglobin
- normocytic, normochromic
Anemia of chronic disease
also known as anemia of chronic inflammation
- inflammation or infectious processes
-cytokines
-RBCs are normochromic, normocytic, hypoproliferative
cause:
body attempts to reduce iron available bacteria
clinical manifestations:
-mild anemia
diagnosis:
- decreased serum iron
treatment:
- focus on underlying chronic condition
anemia chronic disease (tomei)
normacitic, normochromatic: reduced transferring saturation if u were to do a lab test. (usually some type of history, some chronic disease)
Polycythemia Vera
Bone marrow disorder
-too many red blood cells produced
- increased viscosity prevents blood from flowing efficiently, leading to end organ ischemia
-primary vs. secondary polycythemia
-clinical manifestations
increased blood viscosity and volume
headache, dizziness blurred vision
hypertension
thrombi
diagnosis:
- hematocrit over 70
- increased platletes and white blood cells
- decreased iron count
treatment:
- anticoagulation
- therapeutic erythropheresis
- chemotherapeutic approaches
polycythemia vera (tomei)
too many blood cells
hydroxyurea
the drug for sickle cell patients
perfusion
central perfusion
- blood flow pumped by heart to entire vascular system
- cardiac output and blood pressure
- pathologic processes affect entire body
local perfusion (microvascular perfusion)
- volume of blood flowing through specific tissue
- controlled by capillaries serving region
- pathologic processes affect specific tissues
Peripheral Vascular Disease (PVD)
conditions affecting circulation in tissues other than brain or heart
peripheral artery disease (PVD affecting arteries)
common types affecting veins:
- chronic venous insufficiency
- deep vein thrombosis
- leg ulcers
- varicose veins
risk factors:
- smoking
- hypertension, coronary heart disease
- high cholesterol, diabetes
- family history of vascular disease
- obesity, sedentary lifestyle
affects adults over age 50; men more than women
concepts and systems affecting and affected by impaired perfusion
- cognition
-comfort and pain - fluids and electrolytes
- acid-base balance
- nutrition
- oxygenation
arteriosclerosis
- thickening, loss of elasticity
- calcification of arterial walls
atherosclerosis- form of arteriosclerosis caused by plaque buildup
risk factors include genetic and lifestyle components:
-smoking
-hypertension, heart disease
-high levels of cholesterol and LDLs
-diabetes, obesity
-advanced age, physical activity
clinical manifestations:
- myocardial infarction
- stroke
-PAD
diagnosis:
-checking pulses in extremities
-laboratory workup
-hyperlipidemia
-diabetes
-treadmill test with echocardiography
- ankle-brachial index (ABI)
- ultrasonography
-angiography
treatment:
-lifestyle changes
-medication
-surgery to open occluded arteries (angioplasty, stent)
arteriosclerosis (lipid metabolism and lipoprotins)
lipid metabolism:
- dyslipidemia
- hyperlipidemia
-hypercholesterolemia
-hypertriglyceridemia
lipoproteins:
- low-density lipoproteins (LDLs)
- high- density lipoproteins (HDLs)
-triglycerides
vascular diseases and arteriosclerosis (tomei)
people who eat bad, don’t take care of themselves are most susceptible
young people usually means that these vascular disorders are in their family history
why do we want higher HDL? (tomei)
because it takes fat out of our blood and into our liver
when does atherosclerosis begin?
when endothelial cells are damaged
- atheroma
- chronic inflammatory response
-extracellular matrix stabilizes plaque - atheroma intrudes on vessel lumen and impairs cirulation
serum cholesterol and triglyceride values
total cholesterol desirable level should be <200 (mg/dL)
LDL cholesterol desirable level should be 100-129 (mg/dL)
triglyceride desirable level should be <150 (mg/dL)
nonatherosclerotic peripheral arterial disease
group of disorders in which blood flow is decreased for reasons other than plaque buildup
ex:
-coarctation of aorta
- thoracic outlet syndrome
- raynaud disease
causes:
- coarctation of aorta
- thoracic outlet syndrome (TOS)
- raynaud disease
clinical manifestations
-coarctation of aorta: depend on severity of deformity and how quickly symptoms manifest
-thoracic outlet syndrome:
-neck and shoulder region, and down extremity
-pain
-discoloration
-tingling
-weakness
clinical manifestations:
Raynaud disease
- pale skin
- cyanosis
- numbness, tingling, burning sensation
- ischemia (may result in ulceration or tissue necrosis)
diagnosis:
- coarctation of aorta: blood pressure taken on arms and legs
- thoracic outlet syndrome: patient’s reported symptoms, adison maneuver, measures to monitor blood flow
treatment:
-thoracic outlet syndrome (physical therapy)
- raynaud disease (avoidance of triggers, anti-inflammatory medications, calcium channel blockers)
chronic venous insufficiency (CVD)
- most common cause of chronic venous disease
- veins unable to return adequate blood to heart
causes:
-deep vein thrombosis
- varicose veins
associated conditions:
- genetic predisposition
-female gender
-pregnancy
-age over 50 years
-smoking
-lack of physical activity
-obesity
-standing/sitting for long periods
-oral contraceptive use
pathogenesis:
- low pressure in venous system
- squeezing of skeletal muscles surrounding veins
-stretching of veins
-rupture of valves and clot formation
clinical manifestations:
-leg cramps and pain
-edema of leg or ankle
-thickening or discoloration of skin on calves
-heaviness or weakness in legs
common complications/associated conditions:
- leg ulcers
- varicose veins
- deep vein thrombosis (DVT)
Diagnosis:
- assessment of symptoms and triggers
- ultrasound
- venography
- D-dimer test
treatment
preventative measures:
- sclerotherapy
- radiofrequency
- laser ablation
- anticoagulants
- filter in inferior vena cava to trap emboli
venous insufficiency example
calf tendernous, clot from being on a plane for too long
claudications
pain in the leg at rest
hypertension
consistent elevation of blood pressure above 140 mmHg systolic or above 90 mmHg diastolic
- systemic arterial pressure in brachial artery
- local HTN occurs in specific organs
- Pulmonary HTN
causes:
- hypertension creates excess pressure on arterial walls
- arteriosclerosis thickens arterial wall
- categories of blood pressure
primary hypertension:
- no known cause
-accounts for 90% of cases
-factors:
genetics
age
race
diet
smoking and alcohol consumption
sedentary lifestyle
secondary hypertension:
- identifiable cause
factors affecting blood pressure:
- hormones
(renin-angiotension-aldosterone system (RAAS)
- nervous
hypertension contributing factors:
- endothelial dysfunction
-sympathetic nervous system (SNS)
- Alcohol
- Lifestyle factors (increased stress, high salt intake, lack of physical exercise, obesity), genetics
clinical manifestations: long-term consequences
- stroke
- heart failure
-MI
- Chronic kidney disease
- vision loss
- erectile dysfunction
diagnosis
- measurement of blood pressure
nonpharamacologic treatment:
- restrict sodium consumption
- limit alcohol consumption
- stop smoking
- maintain an optimal weight
pharmacologic treatment:
- angiotensin- converting enzyme (ACE) inhibitors
- angiotensin receptor blockers (ARBs)
- calcium channel blockers (CCBs)
- Thiazide diuretics
thoracic outlet syndrome (tomei)
underneath omicron bone (adsons maneuver), manipulate shoulder area to take care of it.
veins: venous insufficiency (tomei)
individuals shouldn’t smoke, they should lose weight, they should wear stockings, shouldn’t be on their feet all the time, elevate their feet)
normal blood pressure
120/80
prehypertensive
systolic: 121-139 mmHg
diastolic: 81-89
stage 1 hypertension
systolic: 140-159mmHg
diastolic: 90-99
stage 2 hypertension
systolic: 160 mmHg
diastolic: 100
structural heart defects (SHDs)
- structural abnormalities that occur during gestation
- abnormal blood flow through heart in postnatal period
-perfusion is the major concept affected by SHDs
congenital heart defects (CHDs)
- grouped into congenital heart disease
- leading cause of birth-defect associated deaths in infants less than 1 year old
-genetic factors
-environmental factors include fetal exposure to:
drugs
alcohol
cigarette smoke
secondhand cigarette smoke
maternal conditions
structure of pediatric cardiovascular system
- exposure to environmental conditions may negatively affect heart development during weeks 6-9 of gestation
- first embryonic heart beat occurs on day 22 of gestation
-by end of 9 weeks gestation, main structures are developed
(any structural defects have already occured)
when is the fetal heart developed
9 weeks
- at the end of 9 weeks gestation, the main cardiac structures are developed, and any defects have already occurred
prenatal and postnatal hemodynamics
fetal circulation
-oxygenated blood enters through umbilical vein
-enters general fetal circulation after bypassing liver
-returns to placenta via umbilical arteries
first breath at birth causes increase in pulmonary pressures
- closure of foramen ovale
-closure of ductus arteriosus by day 21 after birth
- cardiac assessments during the neonatal period may indicate manifestations of CHD
critical congenital heart disease (CCHD)
- serious congenital heart defects
- require surgical correction within first year of life
- screening in first 24-48 hours of life
preductal and postductal pulse oximeter reading
congenital heart defects (CHD)
- alterations in structure of heart chambers, valves, or major vessels
- can lead to development of congenital heart defects
changes affect: blood flow, oxygenation, fluid balance, create immediate or long-term manifestations
pathophysiology of altered blood flow
murmur:
- turbulent blood flow through valve or congenital heart defect
- intensity correlates with size of defect (six-point scale)
CHD classifications:
- increased pulmonary blood flow
- decreased pulmonary blood flow
- obstructed blood flow
- mixed blood flow
increased pulmonary blood flow defects
most common type of CCHD
- pressure gradient between left and right sides of heart (shunt)
atrial septal defect (ASD)
- hole in septum between atria
- allows oxygenated blood from left atrium to shunt to right atrium
treatment: closed heart procedure, open heart procedure
ventral septal defect (VSD)
- hole in septum between ventricles
- small to medium-sized defect (left- to -right shunt)
- large defect (shunting left- to- right and right-to-left)
treatment of large VSD with pulmonary congestions:
- surgical repair
- medical management
patent ductus arteriosus (PDA):
- connection in utero allowing blood to bypass lungs after right ventricular ejection remains open (continues to shunt blood to aorta)
- ductus fails to close in first 48 hours of life
(left-to-right shunt across ductus returning blood to pulmonary circulation)
treatment:
medical management, surgical intervention
decreased pulmonary blood flow defects
obstruction to pulmonary blood flow decreases blood flow to pulmonary circulation (increases pressure on right side of heart)
types:
- tetralogy of fallot
- pulmonary stenosis
- pulmonary atresia
- tricupsid atresia
tetralogy of fallot (TOF)
complication of four defects:
-VSD
-Pulmonary stenosis
-Right ventricular hypertrophy
-overriding aort
cyanosis: right-to-left shunting through VSD
treatment: corrective repair early in infanct, prostaglandins
tetralogy of fallot (tomei)
kids usually bring their knees up to their chest so they can breathe better
pulmonary stenosis (PS)
- narrowing of pulmonary valve
-can occur alone or with other CHD - also known as right ventricular outflow tract obstruction
treatment:
- ductus arteriosus kept open with prostaglandin infusion
- surgical correction
moderate pressure gradient: pulmonary ballon valvuloplasty
severe pressure gradients: pulmonary valvotomy
diagnosis and treatment of critical congenital heart defects
symptoms:
- dyspnea
-tachypnea
-feeding difficulties
-fatigue
-ductus arteriosus
-murmur specific to anomaly
medical management:
- diuretics
- prostaglandins
- antihypertensives
- cardiac glycosides
- inotropes
- respiratory support
surgical intervention:
- if conservative treatment through medications does improve perfusion and oxygenation
factors affecting outcomes:
- age at time of diagnosis
- presenting symptoms
- critical or noncritical CHD
survival rates:
- infants born with noncritical CHD: 97% survive to 1 year of age
- Infants born with CCHD: 75% 1-year survivability
- screening nationwide improves outcomes
diagnosis and treatment of adult congenital heart disorders
- 1 out of 150 adults have some form of defect in structure of heart
- incidence is increasing
- incidence expected to level off by year 2050
causes:
shunt
-ASD
-PDA
-Patent foramen ovale (PFO)
- stenosis
-PS
Complex: acyanotic: transposition of great arteries
cyanotic: TOF, eisenmenger syndrome
diagnostic tests:
- electrocardiography
- chest x-ray
- echocardiography
- CT or MRI scanning
- cardiac catheterization
treatment:
- education
- medication
- surgery
hole in heart (tomei)
fetal heart (pressure will be greater on right side of heart)
- place stethoscope on left side of heart (pressure will be harder on left side of heart?)
**put stethoscope opposite the flow of blood
first heart beat
35 to 37 gestational days (6th gestational week)
new borns (tomei)
24 hours/ has a cardiac evaluation (just to have, for caution)
nurse assessing the child (tomei)
child has to accumulate to the new environment their in (pressure will be building up on the left side of the heart)
-pressure is increasing on left atrial side on initial evaluation, left atrial rises on newborn baby right after birth
newborn has to adjust to air
- in the womb, the blood goes from left to right without going to lungs.
-when fetus is born, then the lungs fill up with air which causes pressure to build up in left side of hart which helps to close that flap/hole in heart= takes 21 days - left atria pressure rises when a newborn baby after birth
alcoholics are deficient in what type of vitamins (tomei) **
folate, vitamin B6, thiamine, and vitamin A
stable angina (tomei)
heart attack without having structural abnormalities
- at activity (physical activity, stress)
- stable angina is a symptom of myocardial ischemia
-usually given nitroglycerine**
unstable angina
can occur at anytime
- chest discomfort or pain caused by an insufficient flow of blood and oxygen to the heart
- may lead to a heart attack
angina is not a…. (tomei)
it is not a heart attack!
- you shouldn’t see any cardiac enzymes elevated
shock
- acute circulatory failure with inadequate or inappropriately distributed tissue perfusion
- inadequate tissue perfusion to meet metabolic needs of cells
- cellular hypoxia and end-organ dysfunction
- imbalance between oxygen supplied and oxygen demands of cells
- inflammatory and clotting cascades
types of shocks
obstructive, cardiogenic, distributive, hypovolemic, septic or anaphylactic
circulatory alterations leading to shock
- heart failure
- low blood volume in circulation
- redistribution of extracellular fluid (ECF) to extravascular sites
- obstruction of blood flow
- blood pressure= cardiac output x systemic vascular resistance
systemic arterial hypotension:
- systolic arterial pressure less than 90 mmHg or mean arterial pressure less than 70 mmHg, tachycardia
clinical signs of tissue hypoperfusion
- cold, clammy skin
- renal output decreases
- altered mental state
- obtundation, disorientation, confusion
- hyperlactatemia
shock is ultimately a deficit of fluid in circulatory system **
compensatory responses strain cardiovascular system:
- increased heart rate and increased sympathetic stimulation
- skin cool and clammy from vasoconstriction
- shunting of fluid away from organs
- left ventricle fails (results in cardiovascular collapse)
pathophysiology of shock
hemodynamics of shock:
- hemodynamics: the forces the heart has to respond to in order to maintain blood flow through the cardiovascular system and supply oxygen to all tissues
factors including circulation:
- blood volume
- systemic vascular tone
- heart rate
- force of contraction
- blood pressure and vascular resistance affect blood flow
multiple organ dysfunction syndrome (MODS):
- resulting hypoxia and decreased oxygen delivery to cells shifts metabolism to anaerobic metabolism
categories of shock
hyovolemic shock (hemorrhagic shock):
- rapid blood or other ECF fluid loss
cardiogenic shock:
- heart unable to maintain adequate cardiac output due to myocardial damage
distributive shock:
- abnormal redistribution of blood
- results from extensive vasodilation and loss of vascular tone
obstructive shock:
- obstruction (blockage) of blood flow
anaphylactic shock:
- acute, life- threatening, IgE- mediated allergic reaction
- occurs on re-exposure in those persons sensitive to an allergen or antigen
stages of shock
stage 1: early, reversible, or compensated shock
(increased heart rate and constriction of blood vessels, activation of renin-angiotensin-aldosterone system (RAAS)
^^ due to response of kidneys to poor perfusion
strong chance of recovery with proper treatment
stage 2: intermediate or progressive shock
- failure of compensatory mechanisms
- decrease in perfusion; leads to cellular hypoxia
- neurologic changes (confusion, disorientation)
- angina, from decreased oxygen delivery to myocardium
- muscular pain
- reversible with prompt treatment
stage 3: refractory or irreversible shock
- declining heart function
- shutdown of kidneys
- injury to cells in organs and tissues throughout body
- death due to multiple organ dysfunction
hypovolemic shock
also called hemorrhagic shock
- loss of more than 15% of body’s fluids
- rapid or excessive loss of significant amount of whole blood
hemodynamic instability
- decreases in tissue perfusion and oxygen delivery
compensatory mechanisms
- address fall in perfusion
- maintain cardiac output
clinical manifestations:
- hypotension SBP < 90 mm Hg
- increase in HR of 15 beats/min within three minutes of standing up
-rapid breathing
-severe shortness of breath
- sudden, rapid heartbeat (tachycardia)
- loss of consciousness
-weak pulse
- sweating
- pale skin
- cold hands or feet
- urinating less than normal or not at all
diagnosis:
- complete blood count
- serum electrolyte concentrations
- blood glucose level
- arterial blood gas
- prothrombin time and partial thromboplastin time
- hemoglobin and hematocrit
- serum lactate concentration and arterial pH
treatment:
- maximize oxygen
- prevent further fluid loss
- replace lost fluids
basic life support
- airway maintenance
- high- flow supplemental oxygen assistance
- cardiopulmonary resuscitation
- fluid resuscitation
- cardiac monitoring
- central venous line
- control of bleeding
- blood products: plasma expanders
- phamacotherapy (calcium, sodium bicarbonate, vasopressor drugs)
cardiogenic shock
- heart unable to circulate adequate amounts of blood
- loss of myocardial function and contractility
- elevations of diastolic filling pressures and volumes
- persistent hypotension
- severe reduction cardiac index
- number one cause of Q-wave myocardial infarction
other causes:
- left-sided heart failure
- blunt cardiac trauma
- myocarditis
- hypertrophic cardiomyopathy
- valvular failure
- acute myocardial infarction (weak heart pumps less blood, increased pressure in left ventricle; increased pulmonary pressure; pulmonary edema, anaerobic metabolism, acidosis and hypoxia)
compensatory mechanisms to correct hypotension and poor perfusion:
- sympathetic nervous system
- RAAS
- ADH system
clinical manifestations:
- cyanosis with cool skin and mottles extremities
- rapid and faint peripheral pulses
- low pulse pressure; tachycardia
- low and distant heart sounds
- peripheral edema and jugular distension
- crackles in lungs
diagnosis:
- first step: diagnose cause of cardiogenic shock to treat appropriately
treatment:
- patent airway maintenance
- fluid resuscitation (unless pulmonary edema)
- pharmacologic therapy (inotropic agens, coronary vasodilators, diuretics, thrombolytics)
- coronary artery revascularization
- correction of acid-base and electrolyte imbalances
- intra-aortic balloon pump
- surgical interventions
- pacemakers and defribillators
distributive shock
impaired distribution of blood flow due to extensive vasodilation and loss of vascular tone
types:
- septic shock
- anaphylactic shock
- neurogenic shock
etiology and pathogenesis:
- anaphylaxis
- adrenal insufficiency
- drug reactions
- hepatic insufficiency
- systemic inflammatory response syndrome
anaphylactic shock
etiology and pathogenesis
- antibody IgE
- histamine and other substances of anaphylaxis
- increased vascular permeability and bronchoconstriction
triggers:
- drugs, foods, and proteins
- animal or insect venoms
- latex
- heavy metal poisoning
- exercise and exposure to cold temperature
clinical manifestations:
- stridor
- tachycardia
- dyspnea, wheezing, coughing
- edema
- laryngospasm, bronchoconstriction
- angioedema, urticaria, pruritus, hives
- gastrointestinal cramps
- hypotension
treatment:
- epinephrine
- patent airway
- beta agonista
- intravenous fluid expanders
- vasopressors
diagnosis:
- shock
- respiratory symptoms
- possible manifestations of anaphylaxis
septic shock
organ dysfunction caused by dysregulated host response to infection
- immunologic, cellular, cardiovascular, hematologic systems overwhelmed
- sequential organ failure assessment (SOFA)
(respiratory status, coagulation status, hepatic status, cardiovascular status, neurologic status, renal status).
qSOFA (organ failure assessment) diagnostic criteria:
- whether patient is in ICU
- respiratory rate > 22/min
- altered mentation
- systolic blood pressure < 100mmHg
treatment:
- perfusion restored with intravenous fluids,
- vasopressors
- 02 support
- broad-spectrum antibitoics
- infection source control
- monitored hourly in ICU:
-central venous pressure, pulmonary capillary wedge pressure, or central venous oxygen saturation - pulse oximetry
- arterial blood gases
- blood glucose, lactate, and electrolyte levels
- renal function
neurogenic shock
caused by blockage of sympathetic nervous system outflow to intrathoracic sympathetic chain
risk factors:
- spinal cord injuries above T6
- brain injury
- barbiturate overdose
- hypoglycemia
- medications
- severe pain
- spinal anesthesia
- vasomotor center depression
difference between spinal shock and hypovolemic shock:
- spinal shock: loss of reflex function below spinal cord injury level; resolves gradually over 4 weeks
- hypovolemic shock: associated with tachycardia
clinical manifestations:
- triad of systolic hypotension, bradycardia, hypothermia
- bradycardia and vascular dilation
- hypoperfusion of organs
- flaccid paralysis below level of injury
- poikilothermia
- priapism
treatment:
- fluid replenishment
- vasopressors
- stabilization of spine and neck
- airway patency
- oxygen therapy
- corticosteroids
- atropine
obstructive shock
obstruction of blood flow to body’s organs
- diagnosed when acute circulatory failure occurs
- rare condition
causes:
- pulmonary embolism
- cardiac tamponade
- tension pneumothorax
clinical manifestations:
- disturbances of consciousness
- oliguria
- hypotension
- tachycardia
- decreased cardiac function and circulatory failure
treatment:
Pneumothorax:
- decrease chest tension or pressure on heart
- needle thoracotomy and pericardiocentesis for pericardial effusion or cardiac tamponade
Pulmonary emboli
- surgical removal of block
- thrombolytic agent
Multiple Organ Dysfunction Syndrome
Progressive organ dysfunction of two or more systems
risk factors: infection, inflammation, acute lung injury, burn, multiple trauma, ischemia, intoxication, iatrogenic factors, idiopathic factors
pathogenesis: tissue injury and multiple organ failure
- Hypoperfusion, hypoxia
- Hyperinflammation, hypercoagulation
- hyperlactemia
- acidosis
- dysregulated immune response
- septic shock
- severity assessment: SOFA
clinical manifestations (6 primary systems):
- respiratory
- renal
- hepatic
- cardiovascular
- gastrointestinal
- neurologic
treatment:
- optimization of hemodynamic, metabolic, immunologic function
- minimization of iatrogenic injury
- fluid resuscitation using volume expanders
- intropic agents
- vasoactive agents
- mechanical ventilation
- protein- rich nutrition
- targeted antibiotics
dystolic heart failure (tomei)
heart is filing, normal ejection fracture
systolic heart failure (tomei)
won’t be ejecting the amount that it should
signs of someone going into shock
- low blood pressure
- altered mental state, reduced alertness and awareness, confusion, sleepiness, cold moist skin, weak or rapid pulse, rapid breathing, hyperventilation, decreased urine output
nurse interventions for shock
- Monitor daily weight for sudden decreases, especially in the presence of decreasing urine output or active fluid loss. Monitor vital signs. Monitor vital signs of patients with deficient fluid volume every 15 minutes to 1 hour for the unstable patient, and every 4 hours for the stable patient. Oxygen administration.
- Keep the person still and don’t move him or her unless necessary. Begin CPR if the person shows no signs of life, such as not breathing, coughing or moving. Loosen tight clothing and, if needed, cover the person with a blanket to prevent chilling. Don’t let the person eat or drink anything.
difference between hypovolemic and cardiogenic shock
The key difference between cardiogenic and hypovolemic shock is that cardiogenic shock arises due to impairment in myocardial performance, making the heart unable to pump enough blood into other parts of the body, while hypovolemic shock arises due to severe blood or body fluid loss, making the heart unable to pump enough blood into other parts of the body.
iron deficiency is most common (tomei)
because iron deficiency is the most common, this doesn’t mean you need to start supplementing their child. this will cause constipation and a lot of other things.
B12 is macrocytic and have neurological issues (tomei)
fetal development (tomei)
mom usually takes 27-37 mg a day for iron supplement
