Patho Exam 2

Question 1

sickle cell anemia

Answer 1

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

Question 2

sickle cell crisis

Answer 2

blood coagulates in the spleen, the eyes could also be affected

**this individual should maintain high volume, drink lots of fluids

Question 3

Thalassemia

Answer 3

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

Question 4

aplastic anemia

Answer 4

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

Question 5

Anemia of chronic disease

Answer 5

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

Question 6

anemia chronic disease (tomei)

Answer 6

normacitic, normochromatic: reduced transferring saturation if u were to do a lab test. (usually some type of history, some chronic disease)

Question 7

Polycythemia Vera

Answer 7

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

Question 8

polycythemia vera (tomei)

Answer 8

too many blood cells

Question 9

hydroxyurea

Answer 9

the drug for sickle cell patients

Question 10

perfusion

Answer 10

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

Question 11

Peripheral Vascular Disease (PVD)

Answer 11

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

Question 12

concepts and systems affecting and affected by impaired perfusion

Answer 12

• cognition
  -comfort and pain
• fluids and electrolytes
• acid-base balance
• nutrition
• oxygenation

Question 13

arteriosclerosis

Answer 13

• 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)

Question 14

arteriosclerosis (lipid metabolism and lipoprotins)

Answer 14

lipid metabolism:
- dyslipidemia
- hyperlipidemia
-hypercholesterolemia
-hypertriglyceridemia

lipoproteins:
- low-density lipoproteins (LDLs)
- high- density lipoproteins (HDLs)
-triglycerides

Question 15

vascular diseases and arteriosclerosis (tomei)

Answer 15

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

Question 16

why do we want higher HDL? (tomei)

Answer 16

because it takes fat out of our blood and into our liver

Question 17

when does atherosclerosis begin?

Answer 17

when endothelial cells are damaged

• atheroma
• chronic inflammatory response
  -extracellular matrix stabilizes plaque
• atheroma intrudes on vessel lumen and impairs cirulation

Question 18

serum cholesterol and triglyceride values

Answer 18

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)

Question 19

nonatherosclerotic peripheral arterial disease

Answer 19

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)

Question 20

chronic venous insufficiency (CVD)

Answer 20

• 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

Question 21

venous insufficiency example

Answer 21

calf tendernous, clot from being on a plane for too long

Question 22

claudications

Answer 22

pain in the leg at rest

Question 23

hypertension

Answer 23

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

Question 24

thoracic outlet syndrome (tomei)

Answer 24

underneath omicron bone (adsons maneuver), manipulate shoulder area to take care of it.

Question 25

veins: venous insufficiency (tomei)

Answer 25

individuals shouldn’t smoke, they should lose weight, they should wear stockings, shouldn’t be on their feet all the time, elevate their feet)

Question 26

normal blood pressure

Answer 26

120/80

Question 27

prehypertensive

Answer 27

systolic: 121-139 mmHg
diastolic: 81-89

Question 28

stage 1 hypertension

Answer 28

systolic: 140-159mmHg
diastolic: 90-99

Question 29

stage 2 hypertension

Answer 29

systolic: 160 mmHg
diastolic: 100

Question 30

structural heart defects (SHDs)

Answer 30

• structural abnormalities that occur during gestation
• abnormal blood flow through heart in postnatal period

-perfusion is the major concept affected by SHDs

Question 31

congenital heart defects (CHDs)

Answer 31

• 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

Question 32

structure of pediatric cardiovascular system

Answer 32

• 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)

Question 33

when is the fetal heart developed

Answer 33

9 weeks
- at the end of 9 weeks gestation, the main cardiac structures are developed, and any defects have already occurred

Question 34

prenatal and postnatal hemodynamics

Answer 34

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

Question 35

congenital heart defects (CHD)

Answer 35

• 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

Question 36

pathophysiology of altered blood flow

Answer 36

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

Question 37

increased pulmonary blood flow defects

Answer 37

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

Question 38

decreased pulmonary blood flow defects

Answer 38

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

Question 39

tetralogy of fallot (TOF)

Answer 39

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

Question 40

tetralogy of fallot (tomei)

Answer 40

kids usually bring their knees up to their chest so they can breathe better

Question 41

pulmonary stenosis (PS)

Answer 41

• 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

Question 42

diagnosis and treatment of critical congenital heart defects

Answer 42

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

Question 43

diagnosis and treatment of adult congenital heart disorders

Answer 43

• 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

Question 44

hole in heart (tomei)

Answer 44

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

Question 45

first heart beat

Answer 45

35 to 37 gestational days (6th gestational week)

Question 46

new borns (tomei)

Answer 46

24 hours/ has a cardiac evaluation (just to have, for caution)

Question 47

nurse assessing the child (tomei)

Answer 47

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

Question 48

newborn has to adjust to air

Answer 48

• 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

Question 49

alcoholics are deficient in what type of vitamins (tomei) **

Answer 49

folate, vitamin B6, thiamine, and vitamin A

Question 50

stable angina (tomei)

Answer 50

heart attack without having structural abnormalities
- at activity (physical activity, stress)
- stable angina is a symptom of myocardial ischemia
-usually given nitroglycerine**

Question 51

unstable angina

Answer 51

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

Question 52

angina is not a…. (tomei)

Answer 52

it is not a heart attack!
- you shouldn’t see any cardiac enzymes elevated

Question 53

shock

Answer 53

• 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

Question 54

types of shocks

Answer 54

obstructive, cardiogenic, distributive, hypovolemic, septic or anaphylactic

Question 55

circulatory alterations leading to shock

Answer 55

• 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

Question 56

shock is ultimately a deficit of fluid in circulatory system **

Answer 56

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)

Question 57

pathophysiology of shock

Answer 57

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

Question 58

categories of shock

Answer 58

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

Question 59

stages of shock

Answer 59

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

Question 60

hypovolemic shock

Answer 60

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)

Question 61

cardiogenic shock

Answer 61

• 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

Question 62

distributive shock

Answer 62

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

Question 63

anaphylactic shock

Answer 63

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

Question 64

septic shock

Answer 64

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

Question 65

neurogenic shock

Answer 65

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

Question 66

obstructive shock

Answer 66

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

Question 67

Multiple Organ Dysfunction Syndrome

Answer 67

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

Question 68

dystolic heart failure (tomei)

Answer 68

heart is filing, normal ejection fracture

Question 69

systolic heart failure (tomei)

Answer 69

won’t be ejecting the amount that it should

Question 70

signs of someone going into shock

Answer 70

• 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

Question 71

nurse interventions for shock

Answer 71

• 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.

Question 72

difference between hypovolemic and cardiogenic shock

Answer 72

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.

Question 73

iron deficiency is most common (tomei)

Answer 73

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.

Question 74

B12 is macrocytic and have neurological issues (tomei)

Question 75

fetal development (tomei)

Answer 75

mom usually takes 27-37 mg a day for iron supplement