NR 507 FINAL EXAM REVIEW Completed with Solutions
Peripheral vascular disease:
PATHOPHYSIOLOGY OF DEEP VEIN THROMBOSIS:
Deep venous thrombosis (DVT)
... [Show More] is clotting of blood in a deep vein of an extremity (usually calf
or thigh) or the pelvis. DVT is the primary cause of pulmonary embolism. DVT results from
conditions that impair venous return, lead to endothelial injury or dysfunction, or cause
hypercoagulability.
Lower extremity DVT most often results from impaired venous return (eg, in immobilized
patients), endothelial injury or dysfunction (eg, after leg fractures), hypercoagulability
Upper extremity DVT occasionally occurs as part of superior vena cava (SVC) syndrome or
results from a hypercoagulable state or subclavian vein compression at the thoracic outlet. The
compression may be due to a normal or an accessory first rib or fibrous band (thoracic outlet
syndrome) or occur during strenuous arm activity (effort thrombosis, or Paget-Schroetter
syndrome, which accounts for 1 to 4% of upper extremity DVT cases).
Deep venous thrombosis usually begins in venous valve cusps. Thrombi consist of thrombin,
fibrin, and RBCs with relatively few platelets (red thrombi); without treatment, thrombi may
propagate proximally or travel to the lungs.
VICHOW’S TRIAD
Three factors are known as Virchow’s
Blood flow
The vessel walls
Blood components
The features of Virchow’s triad
Circulatory stasis – abnormalities of hemorheology and turbulence at vessel bifurcations
and stenotic regions
Vascular wall injury – abnormalities in the endothelium, such as atherosclerosis and
associated vascular inflammation
Hypercoagulable state – abnormalities in coagulation and fibrinolytic pathways and in
platelet function associated with an increased risk of VTE and other cardiovascular
diseases (including CAD and heart failure, and stroke in patients with AF)
Shock:
CAUSES OF HYPOVOLEMIC SHOCKHypovolemic shock results from significant and sudden blood or fluid losses within your body.
Blood loss of this magnitude can occur because of:
bleeding from serious cuts or wounds
bleeding from blunt traumatic injuries due to accidents
internal bleeding from abdominal organs or ruptured ectopic pregnancy
bleeding from the digestive tract
significant vaginal bleeding
Endometriosis
In addition to actual blood loss, the loss of body fluids can cause a decrease in blood volume.
This can occur in cases of:
excessive or prolonged diarrhea
severe burns
protracted and excessive vomiting
excessive sweating
Blood carries oxygen and other essential substances to your organs and tissues. When heavy
bleeding occurs, there is not enough blood in circulation for the heart to be an effective pump.
Once your body loses these substances faster than it can replace them, organs in your body begin
to shut down and the symptoms of shock occur. Blood pressure plummets, which can be lifethreatening.
HOW THE BODY MAINTAINS GLUCOSE LEVELS DURING SHOCK
Our body maintain glucose level during shock by breaking down protein to fuel gluconeogenesis.
The neuroendocrine response to stress is characterized by excessive gluconeogenesis,
glycogenolysis and insulin resistance. Stress hyperglycemia, however, appears to be caused
predominantly by increased hepatic output of glucose rather than impaired tissue glucose
extraction. The metabolic effects of cortisol include an increase in blood glucose concentration
through the activation of key enzymes involved in hepatic gluconeogenesis and inhibition of
glucose uptake in peripheral tissues such as the skeletal muscles. Both epinephrine and
norepinephrine stimulate hepatic gluconeogenesis and glycogenolysis; norepinephrine has the
added effect of increasing the supply of glycerol to the liver via lipolysis. Inflammatory
mediators, specifically the cytokines TNF-α, IL-1, IL-6, and C-reactive protein, also induce
peripheral insulin resistance. In addition, the altered release of adipokines (increased zinc-alpha2
glycoprotein and decreased adiponectin) from adipose tissue during acute illness is thought to
play a key role in the development of insulin resistance
Acid/Base:
CAUSES OF RESPIRATORY ALKALOSIS
Respiratory alkalosis is a disturbance in acid and base balance due to alveolar hyperventilation.
Alveolar hyperventilation leads to a decreased partial pressure of arterial carbon dioxide(PaCO2). In turn, the decrease in PaCO2 increases the ratio of bicarbonate concentration to
PaCO2 and, thereby, increases the pH level.
The decrease in PaCO2 (hypocapnia) develops when a strong respiratory stimulus causes the
respiratory system to remove more carbon dioxide than is produced metabolically in the tissues.
Respiratory alkalosis can be acute or chronic. The chronic form is asymptomatic
The acute form causes light-headedness, confusion, paresthesia, cramps, and syncope. Signs
include hyperpnea or tachypnea and carpopedal spasms. Diagnosis is clinical and with ABG and
serum electrolyte measurements.
Respiratory alkalosis may be produced as a result of the following causes:
Stress
Pulmonary disorder
Thermal insult
High altitude areas
Salicylate poisoning (aspirin overdose)
Fever
Hyperventilation (due to heart disorder or other, including improper mechanical
ventilation)
Vocal cord paralysis (compensation for loss of vocal volume results in overbreathing/breathlessness).
Liver disease
MOLECULES THAT ACT AS BUFFERS IN THE BLOOD
Several substances serve as buffers in the body, including cell and plasma proteins, hemoglobin,
phosphates, bicarbonate ions, and carbonic acid. The bicarbonate buffer is the primary buffering
system of the IF surrounding the cells in tissues throughout the body.
CARBONIC ACID BICARBONATE BUFFER
Cellular respiration produces carbon dioxide as a waste product. This is immediately converted
to bicarbonate ion in the blood. On reaching the lungs it is again converted to and released as
carbon dioxide.
While in the blood , it neutralizes acids released due to other metabolic processes. In the stomach
and duodenum, it also neutralizes gastric acids and stabilizes the intra cellular pH of epithelial
cells by the secretions of bicarbonate ions into the gastric mucosa.
PHOSPHATE BUFFER SYSTEM
Phosphate buffer system operates in the internal fluids of all cells. It consists of dihydrogen
phosphate ions as the hydrogen ion donor ( acid ) and hydrogen phosphate ion as the ion
acceptor ( base ) . If additional hydroxide ions enter the cellular fluid, they are neutralized by the
dihydrogen phosphate ion. If extra hydrogen ions enter the cellular fluid, then they are
neutralized by the hydrogen phosphate ion.PROTEIN BUFFER SYSTEM
Protein buffer system helps to maintain acidity in and around the cells. Hemoglobin makes an
excellent buffer by binding to small amounts of acids in the blood, before they can alter the pH
of the blood. Other proteins containing amino acid histidine are also good at buffering.
Musculoskeletal
IONS THAT INITIATE MUSCLE CONTRACTION
The process of muscular contraction occurs over a number of key steps, including:
Depolarization and calcium ion release
Actin and myosin cross-bridge formation
Sliding mechanism of actin and myosin filaments
Sarcomere shortening (muscle contraction)
Depolarization and Calcium Ion Release
An action potential from a motor neuron triggers the release of acetylcholine into
the motor end plate
Acetylcholine initiates depolarization within the sarcolemma, which is spread
through the muscle fiber via T tubules
Depolarization causes the sarcoplasmic reticulum to release stores of calcium
ions (Ca2+)
Calcium ions play a pivotal role in initiating muscular contractions
Actin and Myosin Cross-Bridge Formation
On actin, the binding sites for the myosin heads are covered by a blocking
complex (troponin and tropomyosin)
Calcium ions bind to troponin and reconfigure the complex, exposing the binding
sites for the myosin heads
The myosin heads then form a cross-bridge with the actin filaments
Sliding Mechanism of Actin and Myosin
ATP binds to the myosin head, breaking the cross-bridge between actin and
myosin
ATP hydrolysis causes the myosin heads to change position and swivel, moving
them towards the next actin binding site
The myosin heads bind to the new actin sites and return to their original
conformation
This reorientation drags the actin along the myosin in a sliding mechanism
The myosin heads move the actin filaments in a similar fashion to the way in
which an oar propels a rowboatSarcomere Shortening
The repeated reorientation of the myosin heads drags the actin filaments along
the length of the myosin
As actin filaments are anchored to Z lines, the dragging of actin pulls the Z lines
closer together, shortening the sarcomere
As the individual sarcomeres become shorter in length, the muscle fibers as a
whole contract
Summary of Muscle Contractions
Action potential in a motor neuron triggers the release of Ca2+ ions from the
sarcoplasmic reticulum
Calcium ions bind to troponin (on actin) and cause tropomyosin to move,
exposing binding sites for the myosin heads
The actin filaments and myosin heads form a cross-bridge that is broken by ATP
ATP hydrolysis causes the myosin heads to swivel and change orientation
Swiveled myosin heads bind to the actin filament before returning to their original
conformation (releasing ADP + Pi)
The repositioning of the myosin heads moves the actin filaments towards the
center of the sarcomere
The sliding of actin along myosin therefore shortens the sarcomere, causing
muscle contraction
GROWTH OF LONG BONES IN CHILDREN
When babies are born, most of their bones are cartilage. This is soft and flexible bone. In adults,
cartilage is still present in the nose and ears, but in the rest of the body it has been replaced by
bone.
As babies grow up, their bones become longer and change from cartilage to proper bone, which
is much harder and durable. Bone growth occurs from the end of the bone, at a place called the
growth plate.
Growth plates are on 'long' bones, e.g. thigh bone (femur) or shin bone (tibia). They are discshaped pieces of cartilage. As cartilage matures, cells called osteoblasts develop with it. The
osteoblasts help to produce new bone, so the bone gets longer.
After a child stops growing (usually in the late teens), the growth plates become calcified, which
means they get thinner and eventually close. After this point, growth of the bones is no longer
naturally possible.
Factors that affect growth
Growth factors are naturally occurring substances. In particular, the liver produces large amounts
of growth factors, which are carried by the blood flow to where they are needed.Growth factors help cells to grow and mature, these processes are known as cell proliferation and
differentiation. They are released by the connective tissue and the bones, where they help the
bones to grow.
Hormones
Hormones are chemical messengers that generally produce slow, gradual effects in the body.
They control many different bodily functions, one of which is growth. They are produced by
organs in the body called glands.
Some hormones act directly on the growth plates themselves, while others stimulate the
production of growth factors, which in turn act on the growth plates. Examples include:
Thyroxine – Produced by the thyroid gland, these hormones regulate protein, fat, and
carbohydrate metabolism as well as the activity of growth hormone. The less thyroxine in
the blood, the slower growth is.
Growth hormone (also known as somatropin) - Very important for growth. From the sixth
month of life until puberty, growth hormone has the greatest impact on growth. It is
produced by a gland in the brain known as the pituitary gland. Growth hormone
stimulates cells to produce growth factors, which causes cartilage cells to multiply and
older cartilage to be transformed into bone. It also helps to burn fat, stimulate the
development of muscles and strengthen the heart function. It may also play a role in
emotional wellbeing.
Sex hormones – These hormones play a really important role during puberty and can
cause growth spurts. Sex hormones promote the production of additional growth hormone
and so increase activity at the growth plates. They also help the cartilage to change into
bone faster and promote bone maturation.
BONES BELONGING TO THE APPENDICULAR SKELETON
The human appendicular skeleton is composed of the bones of the upper limbs, the lower limbs,
the pectoral girdle, and the pelvic girdle. The pectoral girdle acts as the point of attachment of the
upper limbs to the body. The upper limb consists of the arm, the forearm, and the wrist and hand.
There are 126 bones that make up the appendicular skeleton of an adult human. Each limb
contains 30 bones, the pectoral girdle contains four bones, and the pelvic girdle contains two
bones. Articulations, or joints, connect these bones together.
The bones of the appendicular skeletal system are arranged in a manner that allows people to
perform basic functions such as locomotion, gathering food and other objects, and using tools.
These bones are also involved in protection, mineral storage, and production of blood cells and
platelets.
There are four types of bones found in the appendicular skeleton: long bones, short bones, flat
bones, and irregular bones. A long bone is longer than it is wide and has a narrow shaft in themiddle with knobs on each end. Long bones include the collarbones and the bones in the upper
and lower leg, the upper and lower arm, the hand and foot, and the fingers and toes. A short
bone is approximately cube-shaped and includes the kneecap and each bone in the wrist and
ankle. The shoulder blade is an example of a flat bone, which is flat and thin. An irregular bone
does not have a clearly defined shape based on the other categories and includes the bones that
make up the hip. Because bones interact with other bones and are the site of attachment for the
muscle tendons and ligaments that hold bones together, each bone has unique bone markings.81. FORMS OF DYSLIPIDEMIA ASSOCIATED WITH THE DEVELOPMENT OF THE
FATTY STREAK IN ATHEROSCLEROSIS
High LDL
In atherosclerosis, LDL adheres to the injured endothelium and is oxidized by
macrophages to form the fatty streak. Low-density lipoprotein molecules (LDL)
becoming oxidized by free radicals, particularly oxygen free (ROS). When oxidized LDL
comes in contact with an artery wall, a series of reactions occur to repair the damage to
the artery wall caused by oxidized LDL.
82. EVENTS THAT INITIATE THE PROCESS OF ATHEROSCLEROSIS
Vascular endothelial injury can result from atherosclerosis (plaque deposits on arterial
walls). Atherosclerosis initiates platelet adhesion and aggregation, promoting the
development of atherosclerotic plaques that enlarge, causing further damage and
occlusion. Other causes of vessel endothelial injury may be related to hemodynamic
alterations associated with hypertension and turbulent blood flow. Injury also is caused
by radiation injury, exogenous chemical agents (toxins from cigarette smoke),
endogenous agents (cholesterol), bacterial toxins or endotoxins, or immunologic
mechanisms.
83. SIGNS AND SYMPTOMS OF INCREASED LEFT ATRIAL AND PULMONARY
VENOUS PRESSURES IN LEFT SIDED HEART FAILURE
Shortness of breath (dyspnea) when patent exert or when patent lie down
Fatgue and weakness
Swelling (edema) in legs, ankles and feet
Rapid or irregular heartbeat
Reduced ability to exercise
Persistent cough or wheezing with white or pink blood-tnged phlegm
Increased need to urinate at night
Swelling of your abdomen (ascites)
Very rapid weight gain from fluid retenton
Lack of appette and nausea
Difculty concentratng or decreased alertness
Sudden, severe shortness of breath and coughing up pink, foamy mucus
Chest pain if heart failure is caused by a heart atack
Awakening at night with shortness of breath
84. DIFFERENCES BETWEEN LEFT AND RIGHT SIDED HEART FAILURE
Left-sided heart failure: The left ventricle of the heart no longer pumps enough blood
around the body. As a result, blood builds up in the pulmonary veins (the blood vessels
that carry blood away from the lungs). This causes shortness of breath, trouble
breathing or coughing – especially during physical activity. Left side heart failure leads
to a decreased ejection fraction (EF) or systolic heart failure, which is the most common
type of HF. The EF is less than 40% and is abbreviated HFrEF caused by reducedcontractility of the heart muscle. In patients with systolic heart failure, the heart muscle
is thin, enlarged, and distended which makes the heart incapable of sustaining the
necessary cardiac output and tissue perfusion. Left-sided heart failure is the most
common type. Left-sided heart failure is usually caused by coronary artery disease
(CAD), a heart attack or long-term high blood pressure.
Right-sided heart failure: the right ventricle of the heart is too weak to pump enough
blood to the lungs. This causes blood to build up in the veins (the blood vessels that
carry blood from the organs and tissue back to the heart). The increased pressure
inside the veins can push fluid out of the veins into surrounding tissue. This leads to a
build-up of fluid in the legs, or less commonly in the genital area, organs or the
abdomen (belly). Right-sided heart failure generally develops as a result of advanced
left-sided heart failure and is then treated in the same way. It is sometimes caused by
high blood pressure in the lungs, an embolism in the lungs (pulmonary embolism), or
certain lung diseases such as COPD.
85. INFECTIVE ENDOCARDITIS
Infective endocarditis (IE) is an infection and inflammation of the endocardium,
especially the cardiac valves. Bacteria are the most common cause of ineffective
endocarditis with Staphylococcus aureus the most common. Other causes include
streptococci, enterococci, viruses, fungi, rickettsia, and parasites.
Risk factors
• Implantation of prosthetic heart valves
• Congenital lesions associated with highly turbulent flow (e.g., ventricular septal defect)
• Acquired valvular heart disease (especially mitral valve prolapses)
• Previous attack of infective endocarditis
• Intravenous drug use
• Long-term indwelling intravenous catheterization (e.g., for pressure monitoring,
feeding, hemodialysis)
• Implantable cardiac pacemakers
• Heart transplant with defective valve
Clinical Manifestation
The “classic” findings are fever, new or changed cardiac murmur, and petechial lesions
of the skin, conjunctiva, and oral mucosa. Characteristic physical findings include Osler
nodes (painful erythematous nodules on the pads of the fingers and toes) and Janeway
lesions. Other manifestations include weight loss, back pain, night sweats, and heart
failure. CNS, splenic, renal, pulmonary peripheral arterial, coronary, and ocular emboli
may lead to a wide variety of signs and symptoms.
Treatment
The widely accepted Duke criteria for the diagnosis of IE include the two major criteria
of positive blood cultures (at least 2 positive cultures drawn >12 hours apart) andevidence for endocardial involvement (echocardiographic findings of vegetations and
valvular dysfunction or damage), plus minor criteria including predisposing conditions,
fever, evidence of emboli (e.g., Janeway lesions), and immunologic phenomena (e.g.,
Osler nodes).
Musculoskeletal
86. IONS THAT INITIATE MUSCLE CONTRACTION
The process of muscular contraction occurs over a number of key steps, including:
Depolarization and calcium ion release
Actin and myosin cross-bridge formation
Sliding mechanism of actin and myosin filaments
Sarcomere shortening (muscle contraction)
Depolarization and Calcium Ion Release
Calcium ions play a pivotal role in initiating muscular contractions
An action potential from a motor neuron triggers the release of acetylcholine into
the motor end plate
Acetylcholine initiates depolarization within the sarcolemma, which is spread
through the muscle fiber via T tubules
Depolarization causes the sarcoplasmic reticulum to release stores of calcium
ions (Ca2+)
Actin and Myosin Cross-Bridge Formation
On actin, the binding sites for the myosin heads are covered by a blocking
complex (troponin and tropomyosin)
Calcium ions bind to troponin and reconfigure the complex, exposing the binding
sites for the myosin heads
The myosin heads then form a cross-bridge with the actin filaments
Sliding Mechanism of Actin and Myosin
ATP binds to the myosin head, breaking the cross-bridge between actin and
myosin
ATP hydrolysis causes the myosin heads to change position and swivel, moving
them towards the next actin binding site
The myosin heads bind to the new actin sites and return to their original
conformation
This reorientation drags the actin along the myosin in a sliding mechanism
The myosin heads move the actin filaments in a similar fashion to the way in
which an oar propels a rowboat
Sarcomere Shortening The repeated reorientation of the myosin heads drags the actin filaments along
the length of the myosin
As actin filaments are anchored to Z lines, the dragging of actin pulls the Z lines
closer together, shortening the sarcomere
As the individual sarcomeres become shorter in length, the muscle fibers as a
whole contract
Summary of Muscle Contractions
Acton potental in a motor neuron triggers the release of Ca2+ ions from the sarcoplasmic retculum
Calcium ions bind to troponin (on actn) and cause tropomyosin to move, exposing binding sites for the
myosin heads
The actn flaments and myosin heads form a cross-bridge that is broken by ATP
ATP hydrolysis causes the myosin heads to swivel and change orientaton
Swiveled myosin heads bind to the actn flament before returning to their original conformaton
(releasing ADP + Pi)
The repositoning of the myosin heads moves the actn flaments towards the center of the sarcomere
The sliding of actn along myosin therefore shortens the sarcomere, causing muscle contracton
87. GROWTH OF LONG BONES IN CHILDREN
When babies are born, most of their bones are cartilage. This is soft and flexible bone.
As babies grow up, their bones become longer and change from cartilage to proper
bone, which is much harder and durable. Bone growth occurs from the end of the bone,
at a place called the growth plate.
Growth plates are on ‘long’ bones, e.g. thigh bone (femur) or shin bone (tibia). They are
disc-shaped pieces of cartilage. As cartilage matures, cells called osteoblasts develop
with it. The osteoblasts help to produce new bone, so the bone gets longer.
After a child stops growing (usually in the late teens), the growth plates become
calcified, which means they get thinner and eventually close. After this point, growth of
the bones is no longer naturally possible.
Growth factors
Growth factors are naturally occurring substances. In particular, the liver produces large
amounts of growth factors, which are carried by the blood flow to where they are
needed.
Growth factors help cells to grow and mature, these processes are known as cell
proliferation and differentiation. They are released by the connective tissue and the
bones, where they help the bones to grow.
HormonesHormones are chemical messengers that generally produce slow, gradual effects in the
body. They control many different bodily functions, one of which is growth. They are
produced by organs in the body called glands.
Some hormones act directly on the growth plates themselves, while others stimulate the
production of growth factors, which in turn act on the growth plates. Examples include:
Thyroxine – Produced by the thyroid gland, these hormones regulate protein, fat,
and carbohydrate metabolism as well as the activity of growth hormone. The less
thyroxine in the blood, the slower growth is.
Growth hormone (also known as somatropin) – Very important for growth. From
the sixth month of life until puberty, growth hormone has the greatest impact on
growth. It is produced by a gland in the brain known as the pituitary gland.
Growth hormone stimulates cells to produce growth factors, which causes
cartilage cells to multiply and older cartilage to be transformed into bone. It also
helps to burn fat, stimulate the development of muscles and strengthen the heart
function. It may also play a role in emotional wellbeing.
Sex hormones – These hormones play a really important role during puberty and
can cause growth spurts. Sex hormones promote the production of additional
growth hormone and so increase activity at the growth plates. They also help the
cartilage to change into bone faster and promote bone maturation.
88. BONES BELONGING TO THE APPENDICULAR SKELETON
The human appendicular skeleton is composed of the bones of the upper limbs, the
lower limbs, the pectoral girdle, and the pelvic girdle. The pectoral girdle acts as the
point of attachment of the upper limbs to the body. The upper limb consists of the arm,
the forearm, and the wrist and hand. There are 126 bones that make up the
appendicular skeleton of an adult human. Each limb contains 30 bones, the pectoral
girdle contains four bones, and the pelvic girdle contains two bones. Articulations, or
joints, connect these bones together.
The bones of the appendicular skeletal system are arranged in a manner that allows
people to perform basic functions such as locomotion, gathering food and other objects,
and using tools. These bones are also involved in protection, mineral storage, and
production of blood cells and platelets.
Because bones interact with other bones and are the site of attachment for the muscle
tendons and ligaments that hold bones together, each bone has unique bone markings.
There are four types of bones found in the appendicular skeleton: long bones, short
bones, flat bones, and irregular bones.A long bone is longer than it is wide and has a narrow shaft in the middle with knobs on
each end. Long bones include the collarbones and the bones in the upper and lower
leg, the upper and lower arm, the hand and foot, and the fingers and toes.
A short bone is approximately cube-shaped and includes the kneecap and each bone
in the wrist and ankle.
The shoulder blade is an example of a flat bone, which is flat and thin.
An irregular bone does not have a clearly defined shape based on the other categories
and includes the bones that make up the hip. [Show Less]