HESI Prep Flashcards
Risk Factors associated with Osteoporosis-lifestyle
sedentary calcium nutritional deficiency high protein diet excessive alcohol intake excessive caffeine intake smoking
Risk Factors associated with Osteoporosis-drug and disease related
antacids (promote calcium excretion)
Anticonvulsants (promote calcium excretion)
Heparin
corticosteroids or cushing disease (promote calcium excretion)
Gastrectomy
COPD
Malignancy
Hyperthyroidism (accelerate bone turnover)
hyperparathyroidism
Rheumatoid Arthritis
Explain the RANK receptor pathway
(Osteoblasts (formation) produce) RANKL+RANK=osteoclast (resorption) differentiation and proliferation
OPG is a competitor for RANKL receptor site, binds to RANK to block this pathway to keep bone resorption in check with bone formation.
Diverticulosis
the mucosal layer of the colon herniates through the muscularis layer. most often occurs in the sigmoid colon.
Diverticulitis
infected diverticula and abscesses
Symptoms of Diverticulosis
lower left quadrant pain, nausea, vomitng, slight fever, elevated WBC
What irritates diverticulosis?
the lower the volume in the colon, the more vigorous the contractions and thus more pressure on the haustra
age over 40 constipation low dietary fiber connective tissue disorders (marfan syndrome, ehlers danlos) hereditary or genetic predisposition
Risk factors for diverticulosis
Hyperosmolar Hyperglycemic State
aka hyperosmolar Hyperglycemic Nonketotic Syndrome
hyperglycemia blood glucose >600 mg/dL hyperosmolarity blood plasma >320 mOsm/L Dehydration absence of ketoacidosis depression of sensorium
kidneys and glucose
normally, the kidneys try to make up for high glucose levels in the body by allowing the extra glucose to leave the body in the urine. If you do not drink enough fluids, or fluids that contain sugar, the kidneys can no longer get rid of the extra glucose. Glucose levels in the blood can become very high as a result. The blood then becomes much more concentrated than normal, resulting in hyperosmolarity.
Hyperosmolarity
a conditoin in which blood has a high concentration of salt, glucose, and other substances that normally cause water to move INTO the bloodstream. This DRAWS WATER OUT OF ORGANS (including the brain). Hyperosmolarity creates a cycle of increasing blood glucose levels and dehydration.
Risk factors for HHS
type 2 diabetes (insulin resistant kind)
acute pancreatitis
severe infection
myocardial infarction
massive glucosuria brings about what?
water loss as water follows the glucose into the urine
Manifestations of HHS
weakness dehydration polyuria excessive thirst neurological signs- hemiparesis, babinski reflexes, aphasia, muscle fasciculations, hyperthermia, hemianopia (loss of 1/2 visual field), nystagmus, hallucinations, seizures, coma
The onset of HHS is often mistaken for what?
a stroke
type 2 diabetes
most commom
fat, liver, and muscle cells do not respond correctly to insulin=insulin resistance
glucose does not gain access to those cells to provide energy
being overweight makes it harder for your body to utilize glucose properly
Manifestations of diabetes
bladder, kidney, skin infections slow to heal fatigue hunger thirst polyuria blurred vision erectile dysfunction pain or numbness in hands and feet
fasting blood glucose +
> 126 mg/dL twice
hemoglobin A1C test +
> 6.5%
oral glucose tolerance +
> 200 mg/dL two hours after drinking the special drink
Type 1 diabetes
body fails to produce insulin
loss of pancreatic beta cells through autoimmune destruction
osteoporosis
metabolic bone disease characterized by a loss of mineralized bone mass causing increased porosity of the skeleton and susceptibility to fractures
bone resorption outpaces bone formation
decreased intestinal absorption of calcium due to deficient vit D activation
Estrogen deficiency
often leads to osteoporosis
decreased estrogen increases cytokines and decreases OPG
OPG inhibits the RANK receptor pathway which promotes osteoclast differentiation and proliferation
hCG
Human chorionic gonadotropin
in the event of fertilization, hCG is produced by the trophoblastic cells in the blastocyst.
hCG prevents luteal regression.
Corpus luteum
remains functional for three months after fertilization
provides hormonal support for pregnancy until the placenta is fully functional
Anterior pituitary releases FSH and LH
stimulate development of follicles
Starling’s Laww
The maximum force of contraction and cardiac output is achieved when venous return produces an increased in left ventricular end-diastolic filling (preload) such that the muscle fibers are stretched about two and one-half times their normal resting length. When muscle fibers are stretched to this degree, there is optimal overlap of the actin and myosin filaments needed for maximal contraction.
length tension/frank starling mechanism
with increased diastolic filling, there is increased stretching of the myocardial fibers and more optimal approximation of the heads on the thick myosin filaments to the troponin binding sites on the thin actin filaments, this results in increased force for the next contraction
Starling and the Curce
increased contractility=increased CO curve moves up and to the left
decreased inotropy-curve moves down and to the right
heart failure
decreased in CO and renal blood flow leads to increased sodium and water retention, a resultant increase in vascular volume, and venous return to the heart, and an increase in ventricular end-diastolic volume (preload). The heart cant eject all this blood, and the back up accumulates in the lungs and atria.
Name the compensatory mechanisms in heart failure that function together to maintain CO for the failing heart.
frank starling mechanisms
sympathetic reflexes
RAAS
myocardial hypertrophy
why do we give diuretics to people with heart failure?
The use of diuretics in persons with heart failure helps to reduce vascular volume and ventricular filling, thereby unloading the heart and reducing ventricular wall tension.
How does the Frank Starling mechanism hurt heart function?
the increased muscle stretch increases ventricular wall tension and that makes the myocardial muscles consume more oxygen and can then produce ischemia and contribute to further impair inotropy. (curve moves back and to the right)
sympathetic Nervous System role in compensatory response to decreased CO
sympathetic nervous system helps maintain perfusion of the organs by direct stimulation of heart rate and cardiac contractility using EPI and NE, regulating vascular tone, and enhancement of renal sodium and water retention.
sympathetic response is meant to augment blood pressure and CO
When Sympathetic Nervous System compensation goes bad
an increase in sympathetic activity can lead to tachycardia, vasoconstriction, and cardiac arrythmias.
tachycardia and heart failure
tachycardia increases the workload of the heart, increasing oxygen demand and leads to cardiac ischemia and decreased inotropy. Cardiac ischemia and cardiomyopathy both contribute to worsening heart failure.
catecholamines (EPI and NE) and heart failure
prolonged exposure to sympathetic stimulation may lead to desensitization of beta adrenergic receptors without affecting the alpha adrenergic receptors. Even though circulating NE levels are increased in persons with heart failure, the lack of functioning beta adrenergic receptors in relation to alpha adrenergic receptors may lead to vasoconstriction and an increase in systemic vascular resistance.
Why is increased vascular resistance bad in heart failure?
Increased systemic vascular resistance causes an increase in cardiac afterload and ventricular wall stress, thus increasing myocardial oxygen consumption. Other effects include decreased renal perfusion and additional augmentation of the RAAS, which increases blood volume, as well as decreased blood flow to skin, muscle, and abdominal organs.
what is one of the most important effectos of lowered cardiac output in heart failure?
decreased renal blood flow and glomerular filtration rate which leads to sodium and water retention. with decreased renal blood flow, kidneys secrete more renin and circulating levels of angiotensin II increase as well.
Angiotensin II
generalized and excessive vasoconstriction
facilitates release of NE
inhibits reuptake of NE by sympathetic nervous system
stimulates Aldosterone
Increases ADH levels
Aldosterone
increases tubular reabsorption of sodium which results in water retention. aldosterone is metabolized in the liver, and so its levels are further increased when heart failure causes liver congestion.
ADH
vasoconstrictor
water retention
fluid retention and heart failure
the progressive accumulation of fluid leads to ventricular dilation and increased wall tension. This increases oxygen demand and eventually outweighs the compensatory Frank-Starling mechanism, reducing inotropy, and exacerbating heart failure.
angiotensin II and aldosterone and the inflammatory response
stimulate cytokine production (TNF and IL-6)
attract inflammatory cells (neutrophils and macrophages)
activate macrophages at site of injury
stimulate growth of fibroblasts
stimulate synthesis of collagen fibers
—Atherosclerosis!!!!!
tissue plasminogen activator
t-PA released slowly from injured tissues and vascular endothelium converts plasminogen to plasmin which digests the fibrin strands, causing the clot to dissolve=CLOT DISSOLUTION
fibrinolysis
process by which a clot dissolves
tPA is used to treat what?
tPA is the first and only agent approved by the FDA for treatment of acute ischemic stroke. this treatment plan is called thrombolytic therapy. major risk is intracranial hemorrhage of the infarcted brain.
cardiac tamponade
compression of the heart due to accumulation of fluids, pus, or blood in the perocardial sac.
what causes cardiac tamponade
infection, neoplasms, bleeding
cardiac tamponade results in
increased intracardiac pressure, progressive limitation of ventricular diastolic filling, and reductions in stroke volume and cardiac output
pulsus paradoxus
a key diagnostic finding, an exaggeration of the normal variation in the sytemic arterial pulse volume with respiration. In cardiac tamponade, the left ventricle is compressed from within by movement of the interventricular septum and from the outside by fluid in the pericardium. this produces a marked decreased in left ventricular filling and left ventricular stroke volume output.
what indicates tamponade?
a decline in systolic pressure greater than 10 mm Hg during inspiration
treating tamponade
NSAIDS, colchicine, corticosteriods may minimize fluid accumulation
pericardiocentesis-removal of fluid
HDL cholesterol
high density lipoprotein 50% protein the good cholesterol reverse transport of cholesterol by carrying cholesterol from the tissues back to the liver for excretion normal levels 40-60 mg/dL
apoproteins
control the interactions and ultimate metabolic fate of the lipoproteins. the major apoprotein for HDL is apoA-I
Research suggests that genetic defects in apoproteins may be involved in
hyperlipidemia and accelerated atherosclerosis
two sites of lipoprotein synthesis
small intestine
liver-synthesizes and releases VLDL and HDL
ATP binding cassette transporter A class 1 (ABCA1)
specialized lipid transporter that promotes the movement of cholesterol from the tissues and to HDL
defects of ABCA1
Tangier Disease-accelerated atherosclerosis and little or no HDL
HDL inhibits
cellular uptake of LDL by reducing oxidation thereby preventing uptake of oxidized LDL by the scavenger receptors on macrophages
How to increases HDL?
regular exercise
moderate alcohol consumption
certain liquid medications
what decreases HDL?
smoking
the metabolic syndrome
albumin
smallest of the plasma proteins
does not pass through the pores in the capillary wall therefore contributes to plasma osmotic pressure and maintenance of blood volume
serves as a carrier for certain substances and acts as a blood buffer
edema due to decreased capillary colloidal osmotic pressure is usually the result of
a lack of albumin due to liver failure (albumin is synthesized in the liver) or starvation, edema develops because there is a lack of amino acids for plasma protein synthesis
When can you lose plasma proteins?
In kidney diseases like glomerulonephritis, the glomerular capillaries become permeable to albumin and then large amounts of albumin are filtered out of the blood and lost in the urine–edema
burns, or large areas of damaged skin=loss of plamsa proteins–edema
albumin binds and transports
hormones (thyroid 15% T3, T4), fatty acids, bilirubin, and other anions
Thyroid hormone
increases the metabolism and protein synthesis in nearly all tissues of the body
necessary for brain development and growth in infants and small children
causes of heart failure
CAD
hypertension
dilated cardiomyopathy
valvular heart disease
sympathetic nervous system and heart rate
speeds it up
parasympathetic nervous system and heart rate
slows it down
stroke volume is a combination of
preload, afterload, and myocardial contractility
beta adrenergic receptors (EPI and NE=catecholamines bind here)
coupled with cAMP to open L-type calcium channels during inotropy to increase strength of cardiac contraction
digitalis
inhibits the sodium/calcium channel in the myocardium to increase inotropy because calcium builds up inside of the cells
Systolic Ventricular Dysfunction
myocardial contractility is impaired, leading to a decrease in the ejection franction and cardiac output.
Diastolic Ventricular Dysfunction
is characterized by a normal ejection fraction but impaired diastolic ventricular relaxation, leading to a decrease in ventricular filling that ultimately causes a decrease in preload, stroke volume, and cardiac output.
cor pulmonale
High blood pressure in the arteries of the lungs is called pulmonary hypertension. The right side of the heart has a harder time pumping blood to the lungs when this happens. If this high pressure continues, it puts a strain on the right side of the heart, leading to cor pulmonale.
emphysema
loss of lung elasticity and abnormal enlargement of the air spaces distal to the terminal bronchioles, with destruction of the alveolar walls and capillary beds. This enlargement of the air sacs leads to hyperinflation of the lungs and produces an increased in total lung capacity (TLC).
what causes emphysema?
smoking
inherited deficiency of alpha 1 antitrypsin an antiprotesase enzyme that protects the long from injury.
Emphysema is thought to result from the breakdown of elastin (by the enzyme elastase) and other alveolar wall components by enzymes called proteases that digest proteins. These proteases are released from neutrophils, macrophages, and other inflammatory cells. When you smoke (or other irritants) then you cause an influx of inflammatory cells to travel to the lungs, they releases their protein eating enzymes (the proteases) and the enzymes eat the elastic aspect of the lung wall.
Besides smoking, the other major known cause of emphysema is alpha-1 antitrypsin deficiency. However, this is a minor cause of emphysema, compared to smoking.
Alpha-1 antitrypsin (AAT) is a natural protein circulating in our blood. Its main function is to keep white blood cells from damaging normal tissues. White blood cells contain destructive substances they use to fight infections.
Some people – perhaps 100,000 people in the U.S. – have a genetic condition that makes them deficient in alpha-1 antitrypsin. Deficient levels of the AAT protein in the blood allow normal white blood cells to continuously damage lung tissue. If people with AAT deficiency smoke, the damage is even worse.
inherited deficiency of alpha1 antitrypsin
autosomal recessive trait
determined by PI (protein inhibitor) genes
most serious gene mutation is the PIZ gene where you have only 15-20% the alpha 1 antitrypsin you are supposed to.
In its absence, neutrophil elastase is free to break down elastin, which contributes to the elasticity of the lungs, resulting in respiratory complications such as emphysema, or COPD (chronic obstructive pulmonary disease) in adults and cirrhosis in adults or children.
panacinar emphysema
type of emphysema most often seen with the deficiency of alpha1 antitrypsin. produces initial involvementof the peripheral alveoli and later extends to involve the more central bronchioles. Most often in the lower parts of the lung
centriacinar or centrilobular emphysema
most often seen in the upper part of the lung.
Affects the bronchioles in the central part of the respiratory lobule, with initial preservation of the alveolar ducts and sacs. Most common form of emphysema and most often seen in male smokers
addisons disease
primary adrenal insufficiency
adrenal cortical hormones are deficient and ACTH levels are elevated due to lack of feedback inhibition
all layers of adrenal cortex are destroyed
addisons disease manifestations
hyponatremia
loss of extracellular fluid
decreased CO
hyperkalemia
orthostatic hypotension
dehydration
weakness
fatigue
cardiovascular collapse and potential shock
poor tolerance to stress-hypoglycemia, lethargy, weakness, fever, anorexia, nausea, vomiting, weight loss
elevated ACTH causes hyperpigmentation
immunizations
active immunity
memory B and T lymphocytes respond to subsequent exposure to antigens
Rheumatioid Arthrities
a chronic systemic inflammatory disease with bilateral involvement of synovial or diarthrodial joints
pathophysiology of RA
synovial cells line the joint. Inflammatory cells accumulate and cause angiogenesis and pannus to form, which proceed to cover the articular cartilage and isolate it from its nutritional synovial fluid.
pannus
a feature of RA that differentiates it from other forms of inflammatory arthritis. The inflammatory cells found in the pannus have a destructive effect on the adjacent cartilage and bone. Pannus develops over the joint margins leading to reduced joint motion and the possibility of ankylosis.
cellular components of RA
Activated T cell mediated immune response
cytokines released (TNF, IL-1)
Antibody formation
MHC and HLA in RA
MHC genes (major histocompatibility complex HLA human leukocyte antigen on MHC class II molecules with a specific set of HLA DR alleles (DR4, DR1, DR10, DR14) These allesles are thought to form a shared epitope in the hypervariable segemnt of the HLA-DRB1 gene, which forms a rheumatoid pocket on the HLA molecule. the binding properties of this pocket influence the types of peptides that can be bound by the RA-associated HLA-DR molecules, therby affecting the immune response
rheumatoid factor
Ig RF reacts with a fragment of Ig to form immune complexes in persons with RA (Ig RF + IgG. These immune complexes attract neutrophils, macrophages, and lymphocytes to phagocytize them and while they are doing so, they release lysosomal enzymes that destroy joint cartilage. The inflammatory response that follows attracts additional inflammatory cells, setting into motion a chain of events that perpetuates the conditon. as the inflammatory process progresses, synovial cells and subsynovial tissues undergo reactive hyperplasic. Vasodilation and increased blood flow cause warmth and redness. Joint swelling occurs as a result of the increased capillary permeability that accompanies the inflammatory process.
clinical manifestations RA
fatigue anorexia weight loss generalized achiness and stiffness joint manifestations are symmetric and polyarticular. Any diarthridal joint can be affected.
four characteristics must be present to diagnose RA
- morning stiffness for at least 1 hour at least 6 weeks
- simultaneous swelling of thee or more joints for at least 6 weeks
- Swelling of weist, metacapophalangeal, or proximal interphalangeal joints for 6 or more weeks
- symmetric joint swelling for 6 or more weeks
- Rheumatoid nodules
- serum rheumatiod factor identified by a method that is positive in less than 5% of norma subjects
- radiographic changes typical of theumatoid arthritis on hand or wrist radiographs
What antibody presence helps diagnose RA?
Anti-cyclic citrullinated peptide (CCP) antibodies
citrulline-containing proteins may serve as specific targets for the IgG antibody response in RA.
Multiple Sclerosis
inflammation and selective destruction of CNS myelin
HLA-DR2 human leukocyte antigen haplotype
Interleukin 12
responsible for differentiation of T cells; overproduction of IL12 is what causes inflammatory response in MS
oligodendrodytes
built myelin sheath around neuron affected by MS
Insulin
acts to increase protein and lipid synthesis, promotes glucose storage, and inhibits gluconeogenesis or the building of glucose from amino acids
a preventative measure to decrease the risk of developing rheumatic heart disease
is prompt diagnosis of streptococcal infections with a throat culture. Rheumatic heart disease is commonly caused by strptococcal infections.
serum phenylalanine test
a procedure performed on a newborn to decrease the risk of mental retardation and impaired neurological development. Newborn infants are routinely screened within 12 hours of birth to detect high levels of serum phyenylalnine that could cause irresversible mental retardation.
cardiogenic shock
decreased CO, hypotension, hypoperfusion, tissue hypoxia despite adequate inravascular volume. Decreased CO caused by decreased inotropy, increased afterload, or excessive preload.
myocardial damage (infarction, contusion)
sustained arrythmias
acute valve damage, ventricular septal defect
Cardiac surgery
CAD
cardiomyopathy
hypovolemic shock
caused by decreased blood volume loss of whole blood (hemorrhage) loss of plasma (burns) loss of extracellular fluid (vomiting, diarrhea, dehydration) Internal hemorrhage third spacing
Obstructive shock-elevated right heart pressure due to impaired right ventricular fuction
caused by obstruction of blood flow through circulatory system
inability of the heart to fill properly (cardiac tamponade)
Obstruction to outflow from the heart (pulmonary embolus, cardiac myxoma, pneumothorax, or dissecting aneurysm)
Distributive shock
excessive vasodilation with maldistribution of blood flow
loss of sympathetic vasomotor tone (neurogenic shock)
presence of vasodilating substances in the blood (anaphylatic shock)
presence of inflammatory mediators (septic shock)
cardiac tamponade
inability of heart to fill properly
obstructive shock
neurogenic shock
loss of sympathetic vasomotor tone
distributive shock
anaphylatic shock
presence of vasodilating substances in the blood
distributive shock
septic shock
presence of inflammatory mediators
distributive shock
compensatory mechanisms to circulatory shock
sympathetic and renin systems are designed to maintain cardiac output and blood pressure
stimulation of alpha receptors (SNS)
vasoconstriction
stimulation of beta 1 receptors (SNS)
increase heart rate and inotropy
