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Exam (elaborations)

Test Bank - Advanced Physiology & Pathophysiology

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  • Advanced Physiology & Pathophysiology
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  • Advanced Physiology & Pathophysiology

.3 Possible Outcomes of Hepatitis - ANSWER-HBsAg totally cleared = immune stage inactive carrier stage = no injury or inflammation of hepatocytes but patient can suffer from acute flares if virus cannot be cleared and replication continues for >6 months = chronic hepatitis .Absorption A...

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  • September 3, 2024
  • 99
  • 2024/2025
  • Exam (elaborations)
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  • Advanced Physiology & Pathophysiology
  • Advanced Physiology & Pathophysiology
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.3 Possible Outcomes of Hepatitis - ANSWER-HBsAg totally cleared = immune stage



inactive carrier stage = no injury or inflammation of hepatocytes but patient can suffer from acute flares



if virus cannot be cleared and replication continues for >6 months = chronic hepatitis



.Absorption Atelectasis - ANSWER-collapsed lung combined with fluid exudation



alveoli are isolated by a mucous plug and closed pore of Kohn, resulting in atelectasis

∙can fill with stasis fluid caising infection



alveoli in West Zone 3 (lowest lung layer) are the most susceptible to this disorder b/c of their lower
ventilation/perfusion ratio

∙lower ventilation increases the probability of obstruction while higher perfusion increases the chances
of fluid exudation and infection



prevention and treatment is opening the pores of Kohn through deep breaths or positive pressure
breathing which bypasses the mucous plugs and restores ventilation



.Acute Complications of Diabetes - ANSWER-hypoglycemia



diabetic ketoacidosis



hyperosmolar hyperglycemic nonketotic syndrome (HHNKS or HONKS)

,.Acute Respiratory Distress Syndrome (ARDS) - ANSWER-results from diffuse pulmonary endothelial
injury



injury results from exposure to environmental pollutants such as asbestos



injury will cause H2O, solutes and macromolecules to diffuse from intravascular space/capillaries into
lung parenchyma and alveoli → pulmonary edema

∙pulmonary edema many times will co-exist with sepsis, resulting in further lung injury via inflammatory
mediators



ARDS many times signals beginning of multiple organ system failure



.Adrenal Glands - ANSWER-composed of an outer cortex and inner medulla

∙cortex makes up ~80% of weight, composed of 3 distinct layers that produce different hormones



zona glomerulosa is outermost layer and produces mineralocorticoids which regulate the retention of
sodium by the body

∙major minerolocorticoid is aldosterone, which is regulated by the renin-angiotensin system



next later is zona fasciculate, which produces glucocorticoids in response to ACTH stimulation

∙mainly produces cortisol

∙cortisol is involved in carbohydrate metabolism inducing hyperglycemia but also has
immunosuppressant and anti-inflammatory properties

∙also exerts negative feedback on both ACTH from anterior pituitary and CRH from hypothalamus



innermost layer is the zona reticularis, which produces the androgens

∙most DHEA, which can then be converted into other sex steroids



adrenal medulla is composed of chromaffin cells (aka pheochcromocytes) that release catechoalines
epinephrine and norepinephrine directly into blood

,.Adrenocortical Insufficiency - ANSWER-Addison's disease is an autoimmune destruction of the adrenal
glands, resulting in the loss of produced hormones

∙symptoms include muscle weakness, weight loss, low blood sugar and depression from the loss of
cortisol, as well as salt craving and low BP from the loss of aldosterone

∙b/c cortisol is not present, you have the overproduction of ACTH which will lead to hyperpigmentation
of the skin b/c ACTH shares the same first AAs with alpha-MSH



treatment is to replace the missing hormones



.Adrenogenital Syndrome - ANSWER-each class of steroids is converted to their ultimate end product by
a series of enzymes

∙if you knock out one of those enzymes, such as 21beta-hydroxylase, the precursors will be shunted into
another pathway



in congenital adrenal hyperplasia this is what happens

∙patient is no longer able to produce cortisol and instead overproduces DHEA which results in virilization
of the patient, including cliteromegaly, hirsutism and changes in fat and muscle deposition

∙additionally, b/c there is no cortisol to exert negative feedback on the pituitary, ACTH is elevated, which
only exacerbates the problem

∙treatment is to give cortisol, in an effort to restore balance



patients may also have adrenocortical neoplasms → tumors that overproduce DHEA resulting in the
same symptoms

∙removing the tumor is an effective treatment



.Aggregation - ANSWER-irreversible process



reliant on GP IIb/IIIa from activation step

∙recognizes and binds to fibrinogen



the cross-linking of GP IIb/IIIa draws in additional platelets, providing sufficient material for the clot

, ∙additional contractile elements of the platelets actually compact the clot, pulling the damaged tissue
closer together and aiding in the healing process



.Alterations in Refraction - ANSWER-as you grow, so do your eyes



they grow into shape that is most comfortable for whatever you are looking at

∙if you spend a lot of time looking at things up close, the eyes will change shape so that it is easier to
look at things up close



.Amblyopia - ANSWER-lazy eye → blindness of one eye without any physical problem of the eye



brain won't be happy with this and will choose to "ignore" one eye



solution: wear patch over good eye so that brain has to rely on bad eye → bad eye will "come back to
life" since there was no underlying physiological problem with the eye

∙with time, eyes will converge and good vision will be restored



.Anaphylactic shock - ANSWER-caused by generalized IgE hypersensitivity resulting in systemic
vasodilation and increased vascular permeability



pathway

∙antigen enters body, the IgE antibody will recognize antigen and overreact, causing an increase in
inflammatory molecules such as histamine, prostaglandins and kinins to enter via increased capillary
permeability



leads to 3 effects:

∙vasoconstriction of vascular smooth muscle in the GI and other unnecessary organs

∙increased capillary permeability resulting in edema and hypovolemia

∙increased peripheral vasodilation results in decreased SVR/TPR and hypovolemia



end results of hypovolemia: decreased CO and tissue perfusion

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