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QOD Exam 3 Patho Steppe With Complete Questions And Answers
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QOD Exam 3 Patho Steppe With CompleteQuestions And Answers
In one or two sentences, explain the fundamental difference between Type I and Type II
diabetes.
Type I diabetes is characterized by an absolute deficit of insulin due to
immune-mediated destruction of the pancreatic beta cells. Type I diabetes was formally
known as "insulin dependent" or "juvenile diabetes" because of the necessity to take
insulin early on and because it typically manifests at an earlier age.
Type II diabetes is characterized by insulin resistance, meaning there is impaired
peripheral uptake of glucose by cells. Insulin production is actually increased early in
the disease course as the pancreatic cells try to compensate for insulin resistance.
However, over years of chronic insulin resistance, the pancreatic cells undergo
increased stress and will undergo apoptosis, leading to insulin deficit as the disease
progresses.
A patient has a pituitary tumor that secretes excess ACTH. What type of signs and
symptoms would you see in this patient?
A pituitary tumor producing ACTH will lead to excess production of glucocorticoids by
the adrenal glands. This disorder is known as Cushing's disease, which we discussed
way back in our Fluid-electrolyte lecture. NOTE: This is a secondary hormone disorder
because the problem is not occuring in the primary gland. In other words, the adrenal
glands are functioning as normal, but a secondary cause outside the adrenals is
creating the problem. Tumors such as this one tend to be unresponsive to our normal
feedback mechanisms, and therefore contribute to excess hormone production.
Some of the symptoms of Cushing's include:
Hyperglycemia
Fluid and sodium retention
Potassium wasting
Weight gain
Abnormal fat disposition
, Thinning of skin
Accelerated bone loss
Hypertension
Fatigue
There are other too and you can go back to my original fluid-electrolyte slide set to
review those.
Why might a person in DKA have an elevated serum potassium? Why does serum
potassium tend to decrease as we treat DKA?
States of acidosis will cause potassium to shift from the intracellular to the extracellular
space. This is a buffering effect: the cells pull in excess hydrogen ions from the
extracellular space, but in doing so, they must exchange a potassium. The overall effect
is a (generally mild) elevation in potassium.
In DKA, it is not uncommon to see patients come in with mild hyperkalemia. However, as
we treat the patient, the acidosis will resolve. As it resolves, potassium will shift back
into the intracellular space, leading to a drop in serum potassium. Additionally, patients
in DKA usually have polyuria (excess urination), which leads to increased excretion of
potassium. This can lead to a total body depletion of potassium, so we often need to
replace potassium as we continue treatment.
What is the essential difference between epidural and subdural hematomas? What
makes epidural hematomas do dangerous?
Epidural hematomas are arterial bleeds, which means they are higher pressure and will
cause a more rapid accumulation of blood. ICP can rise very quickly with arterial
bleeding.
Subdural hematomas, in contrast, are venous bleeds. While subdural hematomas are
also dangerous and can create life-threatening increase in ICP, they tend to accumulate
slower and can become chronic. They can also be insidious, with blood accumulating
over days. Ultimately, however, both types of hematomas can be fatal if not treated in a
timely manner.
You are taking care of two patients diagnosed with aphasia. You ask each patient how
their day is going. Here are the responses from those patients:
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