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121 Cards in this Set
- Front
- Back
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diabetes
increased or decreased susceptibility to infection? |
increased
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diabetes
increases or decreases phagocyte chemotaxis, adherence, and killing? |
decreased
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diabetes
mechanism of decreased opsonization? |
glycation of C3 inhibits C3 function
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diabetes
increased or decreased opsonin activity? |
decreased
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in diabetes, what does phagocyte function decrease in proportion to?
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the degree of hyperglycemia
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What two mucosal membrane infections are diabetic patients extremely susceptible to? (2)
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1 Candida
2 Saph aureus |
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Diabetes
what complication do polymicrobial foot ulcerations predispose patients to? |
osteomyelitis
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fungal infection other than candida that diabetes are susceptible to?
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rhinocerebral mucormycosis
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what type of ear infection are diabetic patients susceptible to?
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malignant otitis externa
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pseudomonas aeruginosa
diabetic complication that it causes? |
malignant otitis externa
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macro vs microvascular diabetic disease
cerebral vascular disease? |
macro
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macro vs microvascular diabetic disease
carotid artery occlusive disease? |
macro
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macro vs microvascular diabetic disease
peripheral vascular disease? |
macro
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macro vs microvascular diabetic disease
coronary artery disease? |
macro
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type I vs type 2 diabetes
more commonly causes macrovascular disease? |
type 2
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type I vs type 2 diabetes
more commonly causes microvascular disease? |
type 1
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hypercholesterolemia vs hypertryglyceridemia
what is the primary lipid abnormality in diabetes? |
hypertryglyceridemia
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hypertryglyceridemia
how does this contribute to macrovascular disease? |
high FFA levels cause increased production of endothelial cell production of oxygen derived free radicals, endothelin-1, ang II, and inflammatory cytokines
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how does hyperglycemia contribute to macrovascular disease? (this mechanism is complex, but try to walk through it)
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hyperglycemia overloads mitochondria which make ROS's->ROS's inhibit glyceraldyde-3-phosphate dehydrogenase (GAPDH)->without GAPDH activity, glucose shunts into sorbitol, protein kinase C is activated, and AGE's are formed->AGE's activate rage receptors
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macrovascular disease of diabetes
what are the three effects of glyceraldehyde-3-phosphate dehydrogenase inhibition by ROS's? |
1) increased sorbitol production
2) increased PKC activity 3) AGE formation |
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ultimately, what receptors are activated on endothelial cells due to mitochondrial ROS production from hyperglycemia?
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RAGE receptors
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what is the effect of activation of RAGE receptors in macrovascular diabetic disease?
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inflammation
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what transcription factor is activated in endothelial cells in macrovascular disease due to ROSs and AGEs?
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NF-kappa B
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diabetes
increases or decreases coagulability? |
increases
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hyperglycemia
increases or decreases platelet adhesion and activation? |
increases
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what abnormality of the clotting pathway promotes coagulability in hyperglycemia and hyperinsulinemia?
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overproduction of plasminogen activator inhibitor-1 (impaired fibrinolysis)
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what are the two causes of increased plasminogen activator inhibitor-1 in diabetic macrovascular disease? (2)
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1 hyperglycemia
2 hyperinsulinemia |
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diabetic macrovascular disease
increased or decreased endothelial nitric oxide synthesis? |
decreased
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What is the mechanism by which nitric oxide production by the endothelium is reduced in macrovascular diabetic disease?
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NADPH is required for production of NO, and aldose reductase depletes NADPH levels
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RAGE receptors
cause production or degradation of NO? |
degredation
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does nitric oxide depletion in macrovascular diabetic disease cause increased or decreased platelet aggregation?
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increased
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macro vs microvascular disease
nephropathy? |
micro
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macro vs microvascular disease
retinopathy? |
micro
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macro vs microvascular disease
sensory and motor neuropathy? |
micro
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macro vs microvascular disease
autonomic neuropathy? |
micro
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macro vs microvascular disease
dermopathy and foot ulcers? |
micro
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type 1 vs type 2 diabetics
more likely to get microvascular disease? |
type 1
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percent of type 1 diabetics that develop nephropathy?
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50%
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overall, how does the number of type 1 vs type II diabetics being treated for nephropathy compare?
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equal b/c even though type I diabetics are more likely to get nephropathy, there are many more type II daibetics
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nephropathy vs retinopathy
risk increases w/ duration of hyperglycemia? |
retinopathy
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nephropathy vs retinopathy
risk of this complication of diabetes increases at first, but then peaks at 15 to 17 years after diagnosis? |
nephropathy
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nephropathy vs atherosclerosis
risk of this complication of diabetes is proportional to the duration of hyperglycemia? |
atherosclerosis
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what two changes occur in the kidney in diabetic pre-nephropathy? (2)
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1 enlargement of glomeruli/kidneys
2 GFR increased by up to 40% |
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diabetic pre-nephropathy
kidneys shrink or enlarge? |
enlarge
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diabetic pre-nephropathy
increased or decreased GFR? |
increased (up to 40%)
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amyloidosis
increases or decreases kidney size? |
increases
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polycystic kidney disease
increases or decreases kidney size? |
increases
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hypertensive kidney disease
increased or decreased kidney size? |
decreased
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diabetic nephropathy
GBM thins or thickens? |
thickens
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diabetic nephropathy
mesangial proliferation or atrophy? |
proliferation
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what finding is an early strong predictor of the development of diabetic nephropathy?
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increased GFR
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nephropathy
more common in type I or type II diabetics? |
type I
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diabetic nephropathy
initial dilation of efferent or afferent arterioles? |
afferent
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what hormone is thought to cause the dilation of afferent arterioles in diabetic pre-nephropathy?
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IGF-1
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what is the mechanism of increased IGF-1 release that causes afferent arteriole dilation in diabetic pre-nephropathy?
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AGEs bind to RAGE on endothelial cells->endothelial cells make IGF-1
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what cells produce IGF-1 in diabetic pre-nephropathy?
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afferent arteriole endothelial cells
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what is the effect of IGF-1 production in diabetic pre-nephropathy?
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glomerular hyperfiltration
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what is the clinical manifestation of hyperfiltration in diabetic pre-nephropathy?
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microalbuminemia
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microalbuminemia
range of urine albumin amount per 24 hours that fits this dx? |
30-299 mg
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deficiency of what hormone is thought to contribute to hyperfiltration in diabetic pre-nephropathy?
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C-peptide
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C-peptide deficiency
what complication of diabetes is this thought to contribute to? |
hyperfiltration
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what is the consequence of long-term hyperfiltration in diabetic nephrophathy?
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hyalinization of afferent arterioles and glomerulosclerosis (aka Kimmelstiel-Wilson disease)
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24 hour urine albumin is between 30 mg and 299 mg
nephropathy or pre-nephropathy? |
diabetic pre-nephropathy
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24 hour urine albumin greater than 300 mg
nephropathy or pre-nephropathy? |
nephropathy
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what is the first physcial manifestation of diabetic nephropathy?
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dependent pitting edema
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dependent pitting edema
what complication of diabetes is this the first manifestation of? |
nephropathy
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diabetic nephropathy
does GFR increase or decrease in this disease? |
decrease
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How do angiotensin II and AGEs change the composition of the GBM in diabetic nephropathy?
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cause loss of negative charged molecules (sialic acid and heparin sulfate)
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what are the two main negative molecules in the GBM that are lost due to Ang II and AGEs in diabetic nephropathy? (2)
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1 sialic acid
2 heparin sulfate |
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in diabetic nephropathy, what cells respond to hyperfiltration with collagen type IV, laminin, and fibronectin deposition?
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mesangium
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microalbuminuria->macroalbuminuria
is slowing of this progression possible in diabetic kidney disease? |
no
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macroalbuminemia->uremia
is slowing of this progression possible in diabetic kidney disease? |
yes
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what three substances are deposited in the glomerulus by mesangial cells in response to hyperfiltration in diabetic nephropathy? (3)
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1 collagen type IV
2 fibronectin 3 laminin |
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retinopathy vs nephropathy
which occurs first? |
retinopathy
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A diabetic patient without retinopathy presents w/ nephropathy. Is the nephropathy caused by diabetes?
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no, b/c diabetic retinopathy always precedes nephropathy
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what is the single most important step in controlling the progression from macroalbuminemia to uremia in diabetic nephropathy?
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blood pressure reduction
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besides blood pressure reduction, what other two treatments also slow the progression of macroalbuminemia to uremia in diabetic nephropathy? (2)
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1 tight glycemic control
2 cholesterol reduction |
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tight glycemic control effectiveness at slowing of macroalbuminemia progression to uremia
is this treatment more effective in type I or type II diabetes? |
type II
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reduction of what type of blood lipid slows progression from macroalbuminemia to uremia in diabetic nephropathy?
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cholesterol
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DOCs for control of blood pressure in diabetic patients? (2 types)
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1 ACEs
2 ARBs |
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why are ACEs and ARBs the DOCs for treatment of diabetic hypertension?
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they dilate efferent arterioles decreasing glomerular hyperfiltration and pressure
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ARBs and ACEs
dilate afferent or efferent arterioles? |
efferent
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dietary restriction of protein
is this treatment to slow the progression of diabetic nephropathy more effective in type 1 or type II diabetics? |
type 1 diabetics
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what dietary treatment is effective at slowing the progression of nephropathy especially in type I diabetics?
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dietary protein restriction
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sialic acid and heparan sulfate
increased or decreased in the GBM of diabetic patients? |
decreased
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does chronic hyperglycemia increase or decrease production of angiotensin II by glomerular mesangial cells?
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increase
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what hormone/toxic substance combo causes production of growth factors in the mesangium leading to nodular glomeruloslerosis?
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1 ATN II
2 AGEs |
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what toxic substance/hormone combo causes tubulointerstitial fibrosis in patients w/ diabetic nephropathy?
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1 ATN II
2 AGEs |
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What is the mechanism by which AGEs cause tubulointerstitial fibrosis in diabetic nephropathy?
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they are filtered and then absorbed by the proximal tubular cells
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diabetic nephropathy
type of anemia that can develop? |
normocytic normochromic anemia
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mechanism of the normocytic normochromic anemia that can develop in diabetic nephropathy?
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erythropoietin deficiency
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leading cause of blindness in the U.S. between 20 and 65 years of age?
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diabetic retinopathy
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retinopathy
more common in type I or type II diabetes? |
type I
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two stages of diabetic retinopathy? (2)
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1 proliferative
2 nonproliferative |
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what is the first step in the progression of diabetic retinopathy?
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loss of capillary pericytes
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what is the mechanism of microaneurysm formation that is the halmark of non-proliferative diabetic retinopathy?
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loss of pericytes leads to capillary dilatations
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what is the only situation in which NPDR causes visual loss?
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only if cotton wool spots form within the macula causing edema
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what is the hallmark finding of early NPDR?
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microaneurysms
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soft exudates vs hard exudates
early NPDR? |
hard exudates
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soft exudates vs hard exudates
late NPDR? |
soft exudates
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soft exudates
aka? |
cotton wool spots
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dot-blot and flame-shaped hemorrhages vs venous beading
early NPDR? |
dot-blot and flame-shaped hemorrhages
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dot-blot and flame-shaped hemorrhages vs venous beading
late NPDR? |
venous beading
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what two findings predict the progression to the proliferative stage of diabetic retinopathy? (2)
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1 venous beading
2 soft exudates |
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what are two treatment methods that can reduce the risk of progression from NPDR to PDR? (2)
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1 tight glucose control
2 ACE inhibitors |
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percent of type 1 diabetics that develop PDR?
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40%
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what is the most characteristic lesion in proliferative diabetic retinopathy?
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neovascularization
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what is the expected outcome of PDR?
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blindness
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what is the root cause for neovascularizations in PDR?
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ischemia
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what is the primary cause of retinal ischemia in PDR?
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micro-occulusions
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what is the cause of microthrombi formation within the retina in PDR?
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systemic release of PAI-1
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what is the primary pro-angiogenic substance produced in the retina in PDR?
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VEGF
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pigment epithelium derived factor
pro or anti angiogenic? |
anti-angiogenic
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pigment epithelium growth factor
increased or decreased production in PDR? |
decreased
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what two other pro-angiogenic substances are synthesized locally other than VEGF in PDR? (2)
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1 erythropoietin
2 bradykinin |
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erythropoietin
promotes what complication of diabetes? |
PDR
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bradykinin
promotes what complication of diabetes? |
PDR
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new blood vessels in the retina
more or less likely to leak than old capillaries? |
more likely
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what is the result of bleeding of new capillaries in PDR?
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fibrosis->retinal detachment
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what complication if diabetes results if neovascularization obstructs the outflow tract of the anterior chamber?
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neovascular glaucoma
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how does sorbitol production contribute to the pathogenesis of PDR?
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sorbitol accumulation within pericytes causes swelling->lysis of pericytes increases capillary permeability
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