WGU Pathophysiology Study Guide: D236 Pathophysiology Lesson 1 TO Lesson 11
WGU Pathophysiology Study Guide: D236 Pathophysiology Lesson 1 TO Lesson 11:
Pathophysiology Remediation
Lesson 1: Homeostasis Concepts
1. Starling's Law of Capillary forces is the force behind the movements of fl...
Wgu pathophysiology study guide: d236 pathophysiol
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Patho D326
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WGU Pathophysiology Study Guide: D236
Pathophysiology Lesson 1 TO Lesson 11:
Pathophysiology Remediation
Lesson 1: Homeostasis Concepts
1. Starling's Law of Capillary forces is the force behind the movements of
fluid in capillary beds throughout the body. The two forces at work are
hydrostatic and osmotic pressures. Homeostasis is achieved when these
two forces are equal in the capillary- cell interfaces. When the hydrostatic
pressure is high in the bloodstream, fluid is then pushed into the cells and
overflows into the interstitial fluid, causing edema. In a case like
hypoalbuminemia, there is a deficit of albumin protein in the blood. This
lowers the oncotic pressure at work against the hydrostatic pressure,
causing a shift in fluid change. Hydrostatic pressure pushes water into the
cells, causing edema.
2. If hypotension occurs, the kidneys sense decreased perfusion and release
renin. Renin stimulates the liver to release angiotensinogen. This converts
to angiotensin I in the lungs. A specific enzyme, called ACE, converts it into
angiotensin II in the lungs. This angiotensin II causes vasoconstriction,
which increases blood pressure. Angiotensin II also stimulates the adrenal
glands on the kidneys to release a hormone called aldosterone. Aldosterone
helps increase blood volume by increasing sodium and water reabsorption
into the body.
3. Too much potassium in the blood can cause wide QRS complexes and tall,
peaked T waves. This will cause bradycardia, irregular pulse rate, and
cardiac arrest.
4. If pH homeostasis is not maintained, a shift in pH either to the left
(acidosis), or to the right (alkalosis) can occur. Excess H+ molecules can
cause acidosis and excess HCO3- molecules can cause alkalosis. Either one
of these conditions can cause cellular dysfunction and can be fatal.
5. In metabolic acidosis, the lab values would be a pH <3.5 and CO2 <22.
Metabolic alkalosis lab values have a pH >4.5 and CO2 >26. With
respiratory imbalances, it's opposite. With respiratory acidosis, pH is
<3.5 and CO2 is >26. With respiratory alkalosis, pH is >4.5 and CO2 is
<22.
6. A high AG has a value from 16-20 mEq/L and can occur with DKA or lactic
acidosis. The high number of acids consume HCO3-, therefore decreasing
their concentration and increasing the anion gap. In diabetic ketoacidosis,
the unmeasured acids in the blood are called ketones. These ketones break
apart into H+ and keto-anions. Bicarbonate buffers with the H+ ions. With
,this, the bicarbonate decreases in the blood, leaving the keto-anions
numbers to increase. This causes the AG to increase. This is important
because it can help determine the cause of certain metabolic acidosis cases
since not all issues present with an elevated AG. Metabolic acidosis with an
elevated anion gap is found in lactic acidosis, DKA, renal failure, overdose of
aspirin, and ingestion of methanol.
7. Glucose is important to keep at normal levels within the blood because if
too high, called hyperglycemia, it can cause chemical damage to the
endothelial cells that line the
,arteries. This can cause a snowball effect of damage to the kidneys, lower
extremity vessels, and retina of the eyes and can cause atherosclerosis.
With that comes added risks of diseases associated with atherosclerosis like
coronary artery disease, peripheral arterial disease, and cerebrovascular
disease. Hyperglycemia from diabetes creates advanced glycation end
products, further damaging the endothelial lining, stimulating secretion of
endothelin, a vasoconstrictor. This constriction of the vessels is more
common in the lower extremities, causing peripheral arterial disease. This
causes ischemia of the lower extremities and feet which can cause
gangrene and necrosis of the affected tissue.
8. Glucose is the primary source of energy for cells. Glucose needs insulin
to help it enter the cells via insulin receptors. Type 1 Diabetics have had
destruction of their insulin-producing cells, within the pancreas, making it
very difficult for glucose to enter the cells. Type 1 diabetics have glucose
and insulin receptors, just not enough insulin, making them insulin
dependent. Type 2 Diabetics have insulin, glucose, and receptors for
glucose to enter the cells. The issue with type 2 diabetics is that the
receptors are desensitized to insulin, making it difficult for the insulin to
enter the cells.
9. Dialysis is a treatment to help people with kidney disorders to maintain
their fluids, electrolytes, and glucose homeostasis. Dialysis helps to remove
wastes and harmful substances from the blood with a tubing system and a
fluid called dialysate. With renal disease, the kidneys functions decrease,
warranting a multitude of medications to help keep everything functioning
well. When the kidney failure starts to reach a point where the loss of
kidney function is irreversible, dialysis becomes necessary. Some instances
for this are persistent hyperkalemia, uncompensated metabolic acidosis,
and fluid volume excesses.
10.Hemodialysis draws out the patient’s blood into tubes containing
dialysate that filter harmful substances out and returns the clean blood back
to their patient. This is usually required a few times a week and lasts a few
hours each time. Peritoneal dialysis occurs within the patient’s own
peritoneum. The peritoneum is filled with a dialysis solution that also filters
their blood. The fluid sits in the peritoneum for 4 hours, then is drained out
from the cavity and discarded. The dialysate in the peritoneum works with
diffusion to ‘draw’ the harmful substances into the peritoneum until time to
drain. Hemodialysis is more common and better for patients with less
kidney function, although it does have a rigorous schedule. Peritoneal
dialysis can be done at the patient’s home, but must be done everyday
which increases risk for peritoneal infection.
*11. Homeostasis and maintaining optimal physiological health can impact
your wellbeing in a positive way by developing adaptive, compensatory
changes within the cells. If not maintained, you can develop maladaptive
changes, resulting in dysfunctions of cells. If cells are injured too much, cell
death can occur.
,Lesson 2: Cellular Response and Adaptation
1. Innate immunity is the body’s natural defense against pathogens. These
include the skin, mucous membranes, phagocytic cells, ciliated cells, and
the inflammatory response. Adaptive immunity is the body’s “learned”
defense against exposed antigens, using T and B lymphocytes. These
lymphocytes have memory for specific antigens.
2. The adaptive immune system recruits the innate immune system by
relying on toll- like receptors on the surface of cells of the innate system
that detect specific pathogens and stimulate the adaptive response.
3. B lymphocytes are naïve until they encounter antigens. Once exposed to
an antigen, they are stimulated to mature into plasma cells where they can
produce immunoglobulins to attack antigens. This process is why infants and
children initially get sick more often. The young lack the memory cells that
help the body fight off pathogens. Elderly have a decreased population of
naïve T cells, decreasing the potential for strong immune responses.
4. Inflammatory mediators released by white blood cells are called
cytokines. Chemokines are proteins that attract leukocytes to the area of
injury, stimulating the liver to release acute phase proteins that help to
destroy microbes and other foreign material at the site of injury. Kinins and
prostaglandins are released with the injury response, causing the pain
sensation. Histamine is released from mast cells, basophils, and platelets,
which can cause vasodilation and bleeding at the site of injury.
5. If a disease is dominant, it will be expressed even if the person only has
one copy for the disease. If a disease is a recessive, a person will need to
have identical alleles from both parents to obtain the disease. A carrier is a
person who is heterozygous for a recessive allele and doesn’t manifest it.
The dominant allele overcomes the recessive allele. Since the carrier still
passes the recessive allele, it can be passed down to their offspring.
6. In this example, sickle cell allele is represented with an 's'. In the case
of 2 heterozygous carriers of sickle cell disease, the parents' genotypes
would be Ss and Ss. With this heterozygous combination, the probability
of clinical outcomes would be Ss, Ss, SS, and ss. Given these, there's a
25% chance of a genotype to definitely be sickle cell disease.
7. More than 13 alcoholic drinks per month of pregnancy, or more than 2
alcoholic drinks in one sitting, is considered more than minimal levels of
alcohol before a child’s birth. Neurobehavioral Disorder Associated with
Prenatal Alcohol Exposure (ND-PAE) causes thinking and memory issues,
behavioral problems like tantrums, and trouble with daily living activities like
bathing and dressing.
8. Some distinctive features of Down Syndrome are intellectual disability,
slightly slanted eyes, epicanthic eye fold, short nose with a flat nasal bridge,
palmar crease in hands, big space between first and second toes, and
hyperflexible joints. Congenital heart
,disease and blood cancers are common with Down Syndrome. Down
Syndrome is very dependent on maternal age. As a woman ages, their
ability to correctly undergo meiosis can be impaired, increasing the risk for
the disease.
9. Spina bifida is a disorder where some vertebrae over the spinal cord
don’t fully develop and leave some exposed spinal cord. This can occur in
different degrees of severity, with myelomeningocele being the most
severe. The incidence of spina bifida occurring can be minimized by up to
70% when daily folic acid is taken as a prenatal.
10.Cells are adaptive to the environment you place them in until
homeostasis can't be met. There are a few buffer systems that the body
uses to help compensate to make things 'normal' again. If this can't be
achieved, disruptions in the cells occur, causing dysfunction.
Lesson 3: Musculoskeletal Pathophysiology
1. Calcium absorption via the GI tract is facilitated by vitamin D. Vitamin D's
activation is dependent on kidney and parathyroid functions along with
proper sunlight exposure. Hypocalcemia triggers the parathyroid to release
parathyroid hormone, which stimulates the bone to release calcium into the
blood. Calcitonin, a hormone, blocks excess calcium release from bone,
preventing hypercalcemia.
2. Osteocytes are mature cells that maintain metabolism within the bones.
They sit in an area of the bone called the lacunae. Within these lacunae are
little canals that carry nutrients for the bone cells.
3. Bone remodeling is the final step in the bone healing process.
Osteoclasts and osteoblasts are involved in fixing whatever stress was
brought upon the bone. This process can take up to 2 months to
complete. Osteoclasts function in resorbing and degrading existing bone,
to help make room for new bone. Osteoblasts help to build bone up by
secreting osteoid, a bone matrix.
4. Osteoarthritis (OA) is a degeneration of joints caused by aging. Articular
cartilage loss is the first step in joint degeneration. Chondrocytes within the
cartilage are continuously exposed to excessive force, forcing them to
undergo apoptosis. Obesity and repetitive knee/shoulder injuries from
athletes are some examples of excessive force on the cartilage. With loss of
cartilage in the joint, subchondral bone becomes the next part to be
aggravated by such repetitive force, causing osteoblasts and osteoclasts to
become activated. This activation causes microscopic cracks and shearing of
the microvasculature, decreasing blood flow to the subchondral bone.
Inflammation of the synovial membrane within the joint causes enzymes to
leech out and further attack the cartilage.
5. Rickets is a failure of osteoid calcification because of a certain genetic,
nutritional, or metabolic disorder with bone development. Most cases are
due to a vitamin D or calcium deficiency. These deficiencies are more
, common in Africa, Asia, and Europe. The incidence has been high with
breastfed infants and most commonly diagnosed in
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