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NR507 Week 7 Quiz – Chamberlain University – 2024/2025 – Questions with 100% Accurate Answers

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This document contains all quiz questions and 100% accurate answers from Week 7 of the NR507 Advanced Pathophysiology course at Chamberlain University. Covered topics include neurological and musculoskeletal disorders, CNS pathologies, sensory/motor dysfunctions, and related clinical case scenarios. Ideal for mastering Week 7 content and preparing for course exams and Edapt assessments.

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NR507 WEEK 7 QUIZ QUESTIONS WITH 100%
ACCURATE ANSWERS
Diabetes Type I Pathophysiology - Accurate answers Autoimmune-mediated: environmental-
genetic factors tiggers cell-mediated destruction of pancreatic beta cells.
Idiopathic or non-immune: Secondary to other disease like pancreatitis.
Autoantigens bind to beta cells and circulate blood and lymph-->Activation of T helper 1 + 2
lymphocytes-->Macrophages with releases of IL and TNFa, T cytotoxic cells, B lymphocytes to produce
islet cells autoantibodies-->Destruction of beta cells with decreased insulin secretion.


Diabetes Mellitus type 1 Classic Signs - Accurate answers Polydipsia, polyuria, polyphagia, weight
loss, fatigue.


DM Causes - Accurate answers Type I:
Autoimmune: Environmental-Genetic predisposition
Idiopathic: secondary to other disease (ex. pancreatitis)
Type II:
Genetic Predisposition
Obesity
BOTH: Lack of endogenous insulin


Diabetes Insipidus Kidney Function - Accurate answers Nephrgenic DI: inadequate response of the
renal tubules to Anti Diuretic Hormone (ADH). Acquired or genetic. Gradual onset.
Urine output for DI: 8-12 L/Day.


DM chronic complications - Accurate answers Neuropathy
Nephropathy
Retinopathy
Macrovascular Disease
Infection


Commons signs for DM Type I and Type II - Accurate answers Polyuria, polydipsia, fatigue.


DI caused by dysfunction of: - Accurate answers Pituitary System


DI Defined - Accurate answers The inability to concentrate urine and the production of copious
amounts of dilute urine.

, Pancreatic, insulin secreting cells - Accurate answers Beta cells; endocrine gland.


DM End Result on cellular level - Accurate answers Cellular starvation d/t lack of glucose in cells--
>liver stores of glycogen depleted-->use of fat and protein-->Ketones are byproduct of fat catabolism--
>Diabetic Ketone Acidosis (DKA) due to ketone build up
OR if less severe: Prevention of lysis of fats-->No ketone formation-->Hyperglycemic Hyperosmolar
Nonketotic Coma (HHNK).


polydipsia - Accurate answers Excessive thirst.
Elevated blood glucose-->water osmotically attracted from cells into blood-->Intracellular dehydration--
>hypothalmic stim. of thirst.


Polyuria - Accurate answers Excessive urination.
Increased blood glucose=> osmotic diuretic--> amount of glucose filtered by glomerulus is greater than
can be reabsorbed-->glycosuria-->large amounts of water lost in urine.


Polyphagia - Accurate answers Excessive hunger.
Depletion of cellular stores of carbs, fats, and proteins in cellular starvation-->hunger sensation.


Weight Loss in DM type 1 - Accurate answers 1. Fluid loss in osmotic diuresis
2. Loss of body tissue as fat and proteins used for energy d/t insulin deficiency.


Fatigue in DM type 1 - Accurate answers 1. Metabolic changes (poor use of food products)
2. Sleep loss from nocturia


Retinopathy - Accurate answers Retina: most metabolically active structure. Leading cause of
blindness.
Mostly type 2 due to longer hyperglycemia.
Damage to retinal blood vessels and RBCs, platelet aggregation, relative hypoxemia, and HTN.


Stages of Retinopathy - Accurate answers 1. nonproliferative: thickening of retinal capillary
basement membrane, increase in retinal cap perm.=macular edema, vein dilation, microaneursym form,
superfic. and deep hemorrhages.
2. Preproliferative: Retinal ischemia, areas of poor perfusion=infarcts
3. Proliferative: neovascularization (angiogenesis) and fibrous tissue formation within retina or optic
disc.
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