3/24/25, 6:01 NR507 Week 7 Quiz Flashcards |
PM
NR507 WEEK 7 QUIZ AND ANSWERS WITH COMPLETE SOLUTIONS
VERIFIED LATEST UPDATE
Terms in this set (71)
Autoimmune-mediated: environmental-genetic factors tiggers cell-mediated
destruction of pancreatic beta cells.
Idiopathic or non-immune: Secondary to other disease like pancreatitis.
Diabetes Type I Pathophysiology 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 Polydipsia, polyuria, polyphagia, weight loss, fatigue.
Type I:
Autoimmune: Environmental-Genetic predisposition
Idiopathic: secondary to other disease (ex. pancreatitis)
DM Causes Type II:
Genetic Predisposition
Obesity
BOTH: Lack of endogenous insulin
Nephrgenic DI: inadequate response of the renal tubules to Anti Diuretic Hormone
Diabetes Insipidus Kidney Function (ADH). Acquired or genetic. Gradual onset.
Urine output for DI: 8-12 L/Day.
Neuropathy
Nephropathy
DM chronic complications Retinopathy
Macrovascular Disease
Infection
Commons signs for DM Type I and Type II Polyuria, polydipsia, fatigue.
DI caused by dysfunction of: Pituitary System
The inability to concentrate urine and the production of copious amounts of dilute
DI Defined
urine.
Pancreatic, insulin secreting cells Beta cells; endocrine gland.
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
DM End Result on cellular level Acidosis (DKA) due to ketone build up
OR if less severe: Prevention of lysis of fats-->No ketone formation-->Hyperglycemic
Hyperosmolar Nonketotic Coma (HHNK).
Excessive thirst.
polydipsia Elevated blood glucose-->water osmotically attracted from cells into blood--
>Intracellular dehydration-->hypothalmic stim. of thirst.
Excessive urination.
Increased blood glucose=> osmotic diuretic--> amount of glucose filtered by
Polyuria
glomerulus is greater than can be reabsorbed-->glycosuria-->large amounts of
water lost in urine.
Excessive hunger.
Polyphagia Depletion of cellular stores of carbs, fats, and proteins in cellular starvation-->hunger
sensation.
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, 3/24/25, 6:01 NR507 Week 7 Quiz Flashcards |
PM
1. Fluid loss in osmotic diuresis
Weight Loss in DM type 1
2.Loss of body tissue as fat and proteins used for energy d/t insulin deficiency.
1. Metabolic changes (poor use of food products)
Fatigue in DM type 1
2.Sleep loss from nocturia
Retina: most metabolically active structure. Leading cause of blindness.
Mostly type 2 due to longer hyperglycemia.
Retinopathy
Damage to retinal blood vessels and RBCs, platelet aggregation, relative hypoxemia,
and HTN.
1. nonproliferative: thickening of retinal capillary basement membrane,
increase in retinal cap perm.=macular edema, vein dilation, microaneursym form,
superfic. and deep hemorrhages.
Stages of Retinopathy
2.Preproliferative: Retinal ischemia, areas of poor perfusion=infarcts
3.Proliferative: neovascularization (angiogenesis) and fibrous tissue formation within
retina or optic disc.
Excessive accumulation that causes intracellular osmotic pressure-->excess water
Sorbitol in DM type 2 in tissues-->macular edema, cataracts; decreased nerve conduction; swollen, stiff
RBCs which decrease circulation.
Diabetic kidney disease (DKD).
50% of people with DM develop DKD.
Nephropathy glomeruli injured by protein denaturation, high renal blood flow d/t hyperglycemia,
RAAS activation-->intraglomerular HTN-->increased protein excretion-->glomerular
damage-->decreased GFR.
Most common complication of DM. Nerves don't need insulin for glucose transport
and are vulnerable to chronic hyperglycemia.
Neuropathy
50% of DM type 2 have Periph Neuro.
Nerve degeneration begins at peripheral and moves to spine.
2/
8
PM
NR507 WEEK 7 QUIZ AND ANSWERS WITH COMPLETE SOLUTIONS
VERIFIED LATEST UPDATE
Terms in this set (71)
Autoimmune-mediated: environmental-genetic factors tiggers cell-mediated
destruction of pancreatic beta cells.
Idiopathic or non-immune: Secondary to other disease like pancreatitis.
Diabetes Type I Pathophysiology 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 Polydipsia, polyuria, polyphagia, weight loss, fatigue.
Type I:
Autoimmune: Environmental-Genetic predisposition
Idiopathic: secondary to other disease (ex. pancreatitis)
DM Causes Type II:
Genetic Predisposition
Obesity
BOTH: Lack of endogenous insulin
Nephrgenic DI: inadequate response of the renal tubules to Anti Diuretic Hormone
Diabetes Insipidus Kidney Function (ADH). Acquired or genetic. Gradual onset.
Urine output for DI: 8-12 L/Day.
Neuropathy
Nephropathy
DM chronic complications Retinopathy
Macrovascular Disease
Infection
Commons signs for DM Type I and Type II Polyuria, polydipsia, fatigue.
DI caused by dysfunction of: Pituitary System
The inability to concentrate urine and the production of copious amounts of dilute
DI Defined
urine.
Pancreatic, insulin secreting cells Beta cells; endocrine gland.
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
DM End Result on cellular level Acidosis (DKA) due to ketone build up
OR if less severe: Prevention of lysis of fats-->No ketone formation-->Hyperglycemic
Hyperosmolar Nonketotic Coma (HHNK).
Excessive thirst.
polydipsia Elevated blood glucose-->water osmotically attracted from cells into blood--
>Intracellular dehydration-->hypothalmic stim. of thirst.
Excessive urination.
Increased blood glucose=> osmotic diuretic--> amount of glucose filtered by
Polyuria
glomerulus is greater than can be reabsorbed-->glycosuria-->large amounts of
water lost in urine.
Excessive hunger.
Polyphagia Depletion of cellular stores of carbs, fats, and proteins in cellular starvation-->hunger
sensation.
1/
8
, 3/24/25, 6:01 NR507 Week 7 Quiz Flashcards |
PM
1. Fluid loss in osmotic diuresis
Weight Loss in DM type 1
2.Loss of body tissue as fat and proteins used for energy d/t insulin deficiency.
1. Metabolic changes (poor use of food products)
Fatigue in DM type 1
2.Sleep loss from nocturia
Retina: most metabolically active structure. Leading cause of blindness.
Mostly type 2 due to longer hyperglycemia.
Retinopathy
Damage to retinal blood vessels and RBCs, platelet aggregation, relative hypoxemia,
and HTN.
1. nonproliferative: thickening of retinal capillary basement membrane,
increase in retinal cap perm.=macular edema, vein dilation, microaneursym form,
superfic. and deep hemorrhages.
Stages of Retinopathy
2.Preproliferative: Retinal ischemia, areas of poor perfusion=infarcts
3.Proliferative: neovascularization (angiogenesis) and fibrous tissue formation within
retina or optic disc.
Excessive accumulation that causes intracellular osmotic pressure-->excess water
Sorbitol in DM type 2 in tissues-->macular edema, cataracts; decreased nerve conduction; swollen, stiff
RBCs which decrease circulation.
Diabetic kidney disease (DKD).
50% of people with DM develop DKD.
Nephropathy glomeruli injured by protein denaturation, high renal blood flow d/t hyperglycemia,
RAAS activation-->intraglomerular HTN-->increased protein excretion-->glomerular
damage-->decreased GFR.
Most common complication of DM. Nerves don't need insulin for glucose transport
and are vulnerable to chronic hyperglycemia.
Neuropathy
50% of DM type 2 have Periph Neuro.
Nerve degeneration begins at peripheral and moves to spine.
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8
