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111 Cards in this Set
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What is the difference between "absolute" and "relative" insulin deficiency?
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Absolute= complete loss of insulin (ex: pancreatectomy)
Relative= defects in insulin action (not complete loss) |
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What is the difference in blood sugar and insulin excursions in normal vs. diabetic patients?
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Normal- Insulin peaks to 500x basal, Glucose 70x basal
Diabetic- Insulin excursion get SMALLER, and glucose excursions in blood sugar INCREASE. |
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What are the four major criteria for diagnosis of Diabetes Mellitus (DM) according to the American Diabetic Assoc.?
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- Plasma glucose > 200 mg/dl at any time + classic symptoms
- Fasting Plasma glucose (FPG) >126 mg/dl (more than 8 hrs after last meal) - 2 hr plasma glucose >200mg/dl during oral glucose tolerance test (OGTT) - HbA1C >6.5 |
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What are the classic triad of symptoms of diabetes mellitus (in non-pregnant people)?
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- Polyuria (urination increase)
- Polydipsia (increase thirst) - Unexplained weight loss |
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What is HbA1c?
Why is it possible to take this level at any time of the day, during doctor's visit, fasting or non-fasting? |
Glucose added to N-terminal valine of hemoglobin. It is done non-enzymatically (thus doesn't rely on enzyme kinetics).
It gives you the "integrated" glucose conc. over life span of RBC (3 mo) - doesn't matter if you're fasting or not, always 1:1 ratio of RBC and glucose |
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How is Hgb1Ac measured today? How was it measred in the past?
What are normal values and diabetic criteria? |
Past- chromatography
Today: Capillary electrophoresis, Affinity chromatography, Immunoassay normal = 5.4 +/- 0.6 (4.8 to 6) diabetes >6.5 |
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What is Pre-diabetes?
Why does it apply only to T2DM? |
Individuals w/ abnormal number, BUT who are not sufficiently abnormal to warrant dx of T2DM. *important to diagnose so they can PREVENT!
T1DM has a different pathophysiology (it is not preventable by lifestyle changes, one either has it or doesn't). |
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What are the values for FPG, OGTT, and Hgb 1A that correlate with Pre-Diabetes?
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FPG: 100-125 mg/dl
OGTT-2h: 140-199 Hgb 1A: 5.7 to 6.4% *note ~10% of people are progressing to T2DM per year! |
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Briefly describe the following types of diabetes:
Type 1A Type 1B Type 2 |
Type 1A: Immune mediated, with destruction of B cells
Type 1B: Insulin deficient (NOT autoimmune) Type 2: Insulin resistance + Insulin secretory deficiency |
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What is Gestational Diabetes?
What are some risk factors for babies born to mothers with GD? |
Hyperglycemia acquired during pregnancy (that then resolves).
It puts baby at risk for obesity (glucose from mom gets to fetus, stimulates insulin secretion and growth), labor defects (shoulder dystocia), and higher risk of T2DM as an adult. |
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What is Secondary DM?
What about Monogenic DM? |
Secondary= secondary to some other cause. Cystic fibrosis (fibrosis of pancreas affecting B cells), drug induced, mitochondrial defects
Monogenic: from single gene mutations. Ex: MODY, signaling defects, insulin gene mutation |
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What is MODY?
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Maturity Onset Diabetes of the Young
- Autosomal dominant - multiple types - monogenic disorder - usually defects in transcription factors and Glucokinase |
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A patient comes to you as a referral because she has hyperglycemia. She has a normal physical exam except for hearing loss (she wears hearing aids) and a Family history of a brother with neuromuscular problems. Her pediatrician refered her to you because he was puzzled that despite being skinny, she has what seems to be Type 2DM.
What is going on? |
She has Diabetes associated with Mitochondrial disease-
- sensorineural hearing loss - family members with mitochondrial disease - not classic T2DM with obesity |
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What is the typical onset of Diabetes Type 1? Type 2?
How are they different in terms of their genetics? |
Type 1< 20 yrs (young ppl)
Type 2 >30 yrs (older ppl) Type 1: HLA-D linked, ~50% twin concordance Type 2: no HLA association, 90-100% twin concordance |
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How is the pathogenesis of Type 1 vs. Type 2 differ?
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Type 1: autimmune, sever insulin deficiency
Type 2: Insulin resistance and relative insulin deficiency |
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T or F
Epigenetics, Culture, and Environment all play a role in the onset of Diabetes Mellitus. |
True!
Ex: NH groundwater with arsenic in it, has been associated with T2DM. |
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What causes Type1 Diabetes?
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Combination of genetic, environmental, immunologic factors. Autoimmune process may be triggered by infection.
Loss of B-cell mass over years |
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T of F
T1DM is synonymous with Juvenile Diabetes because children tend to develop it when they are young. |
False
Adolescent is peak age at diagnosis (stress, puberty), but it can be diagnosed throughout life. Juvenile-Diabetes= outdated term |
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What is the "Honeymoon Period" associated with Type 1 Diabetes?
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After some insulin replacement is given, you start recovering some Beta cell mass. But then it declines and goes to absolute insulin deficiency.
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Even if someone is taking exogenous insulin supplementation and goes into a "honeymoon" phase, how can you determine the intracellular concentration of insulin?
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C-peptide (it's an indicator of endogenous insulin production). Not affected by exogenous intake.
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What is Insulitis and with why diabetes type do we see it?
Circulating immunologic markers to what three things might be seen in patient's with this condition? |
Type 1- lymphocytic infiltration of pancreas. causes insulin deficiency. Beta cells destroyed and atrophy.
Targets: 1. insulin 2. glutamic acid decarboxylase (GAD) 3. ICA-512 (islet cell antigen) |
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What is the primary defect causing T2DM?
What PREVENTABLE condition is the disease strongly correlated with? |
Trick question! Primary defect is UNKNOWN.
Strong correlation with Obesity. First line treatment = lifestyle changes (then Metformin) |
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What happens over time to the Insulin sensitivity and the Insulin secretion in Type 2 Diabetes?
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Over time: Insulin sensitivity decreases (inc. insulin resistance)
Insulin secretion decreases over time. |
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What are some acute complications of DM?
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DKA (diabetic keotacidosis)
HHS (hyperglycemic Hyperosmolar State) - Iatrogenic, hypoglycemia |
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What are some chronic complications of DM?
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Microvascular= (eye, neuro, nephro)
Macrovascular= (coronary heart disease, perihperal arterial disease, cerebrovascular |
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T or F
The tighter the control of HB1Ac, the better! |
True
*however too much tight control give risk for hypoglycemia |
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What clinical signs would put someone into the spectrum of Diabetic ketoacidosis?
With which type of diabetes is this more closely associated? |
Nausea, Vomiting, Confusion, Coma
*more closely associated with T1DM |
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What physical exam components would you want to check for in the assessment of pts with T1DM?
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*make sure to get full history
Also signs of dehydration & autoimmune thyroiditis (increased chance of having autoimmune disease against pancreas) |
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What is an "artificial pancreas"?
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An implantable insulin pump + a continuous glucose monitor. This will eliminate need for pts to constantly monitor blood glucose and administer insulin.
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What is the target Hgb A1C, preprandial glucose, and postprandial glucose for Adults with Type 1 or Type 2 diabetes?
What should their blood pressure and lipid profile look like? |
Hgb A1c <7%
Preprandial 70-130 Peak post-prandial <180 BP <130/80 Lipids- generally normal LDL, HDL, TG |
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What are some emerging treatment modalities for Type1 and Type 2 Diabetes?
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Type 1-
1. pancreas transplant (and renal transplant) 2. Islet cell transplant 3. BCG tb vaccine (immunomodulatory) Type 2 - Bariatric surgery (if morbidly obese >35) |
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A 32 year old, normal weight woman presents with a 2 month hx of polyuria, polydipsia, and weight loss (unexplained). A random serum glucose is 228 mg/dl. Her younger sister has celiac disease. Family hx is negative for diabetes. Most likely diagnosis is...
a. type 1 b. type 2 c. monogenic d. unknown-further testing required |
A. Type 1
Sibling has history of autoimmune condition. She is not overweight or has risk factors for Type 2 (obesity, etc.) |
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Which of the following is adequate to make a diagnosis of diabetes?
a. Random glucose >200 mg/dl in a person with no symptoms of diabetes b. A fasting serum glucose of 105 mg/dl c. overt symptoms (polyuria, polydipsia, weight loss) and a random glucose of 150 mg/dl d. A hemoglobin A1c of 7% |
D. Hemoglobin A1C (>6.5% = diabetes)
The rest are not within range (FSG >126, Random glucose >200 with sxs) |
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Which of the following is characteristic of T1DM but not T2DM?
a. symptoms of hyperglycemia b. twin concordance of approx. 50% c. Insulin resistance d. mutation in Insulin gene |
B. Twin concordance ~50% in Type 1 (in type 2 it's 90-100%)
mutation in insulin gene is just one example of MONOGENIC Diabetes (different type all together). |
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What is the incidence of Diabetic Ketoacidosis?
Why is the mortality today so much less than it was in the 1900s? |
2-5 cases/ 100 patients with T1DM
Mortality is now 1-2.5% because we have the ability to measure and correct for electrolytes |
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What would the levels of the following electrolytes be in a person with diabetic ketoacidosis:
Na K Glucose HCO3 pCO2 |
Na decreased (hyponatremia)
K increased (serum hyperkalemia, but can become hypokalemic) Glucose- >600 HCO3 decrease pCO2 decrease |
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What is the treatment for DKA?
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IV fluids with Na replacement
Intravenous Insulin make sure to start K+ replacement (only give bicarb if necessary) |
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Why does a person with DKA breath in a heavy labored style?
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Kussmaul breathing- rapid respiratory rate- hyperventilating to release CO2 (due to acidotic buildup).
That is why pCO2 is low. |
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What type of diabetes is DKA more closely associated with?
What pH is considered acidotic? |
Type1 Diabetes more common (BUT it can happen in Type 2 with poor glycemic control)
pH less than 7.4 is acidotic |
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Describe the vicious cycle that patients who have DKA get into?
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Low insulin --.hyperglycemia and metabolic derrangements --> increased stress and increased counter-regulatory hormones-->further increase insulin defects
cycle goes on |
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What produces Hyperglycemia in the DKA patient?
What produces ketosis in the DKA patient? |
Insulin deficiency (decreased glucose disposal)
Increased counter reg hormones (increased hepatic glucose synthesis) Ketosis Insulin deficiency (decreased FA synthesis, increased lipolysis) Glucagon (increased liver ketogenesis) |
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Why does Acetyl coA get shunted into the ketogenic pathway during FASTING state?
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Fasting state uses up O.A.A for gluconeogenesis. Low insulin prevents Acetyl coA from being built up into stored Fat.
Acetyl CoA increases from fat breakdown and overwhelms ability to be used in TCA. Thus the liver converts it to ketone bodies. |
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What causes osmotic dieuresis in the DKA patient?
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Glucose and ketone bodies are building up in the ECF, they attract water and also overwhelm kidneys which get rid of them (peeing a lot, Glucose and Ketone bodies in urine!)
*note, this loss of ECF also causes dehydration |
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What causes hyponatremia in a DKA patient?
What about HYPERkalemia? |
Since glucose concentration increasing in ECF (and more water being lost), water flows out from ICF to ECF. This causes Na concentrations to dilute- dilutional hyponatremia.
Insulin usually causes K+ to enter cell, without it, K+ will leave the cell (and you will have high potassium levels). |
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Is the anion gap increased or decreased in DKA? why?
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INCREASE
cation - anion. HCO3 decreases, so does Cl- due to electrolyte loss. So anion gap increases. |
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Why can a person in DKA get glucose levels that sometimes exceed 600?
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If a person becomes severely dehydrated (losing water and electrolytes AND vomitting from irritation caused by ketones), they will become hypotensive. Kidney cannot function to get rid of glucose and ketone so glucose level rises even more! and pt becomes even more ketotic/acidotic.
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What types of things precipitate DKA?
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Infection, stress (can be lifestyle stress!), insulin deficiency (non-compliance!). Sometimes if patient has new diagnosis and has not been managed yet.
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Why does a person with DKA develop thirst, blurred vision, weakness, and weight loss?
What is the cause of the fruity odor of patients with DKA? |
Thirst- loss of water, blurred vision (osmotic effect on lens), weakness (electrolyte imbalance), weight loss (due to vomitting, starvation state, water loss)
Fruity odor comes from the acetoacetate being converted to acetone (volatile compound). |
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T or F
All patients with DKA are potassium depleted. |
True!
They might be hyperkalemic (because ECF has high K) but that is coming from their ICF and if you don't supplement with K, when they get insulin corrected, K will rapidly fall and they will become hypokalemic. |
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Why does one give dextrose after a person who is being treated for DKA gets to a slightly lower serum glucose?
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You don't want to make them hypoglycemic (remember, you're pumping insulin in). So you want to add dextrose.
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What is the current practice on using Bicarbonate administration to treat DKA?
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Typically not done except in EXTREME cases (pH <7, hypotensive and not responding to fluid, Respiratory depression).
It can increase risk of hypokalemia! |
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What type of diabetes is Hyperosmolar Hyperglycemic State (HHS) typically associated with?
What sorts of things can precipitate this condition? |
HHS more associated with T2DM
Diuretics (hyperosmolarity) and infection can often precipitate this condition. |
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What are the key differences between HHS and DKA?
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HHS- really high glucose, hyperosmolarity, NO SIGNIFICANT KETOSIS! (no vomiting, fruity odor, etc.)
no severe anion gap! no decrease in HCO3! |
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What is the treatment for patients with HHS?
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Restore volume (be careful of overloading patients!)
Provide insulin to patients (they are much more sensitive to it). Be careful of rapid shift of extracellular fluid to intracellular space |
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For patient's with Diabetes, what are the MNT (medical nutrition therapy) recommendations for:
- Carbs - Total dietary fat - Proteins |
Carbs- 45-60% (carb counting, low glycemic index)
Dietary fat- <30% (limit saturated fat, low trans fat, add fish) Protein- 15-20% (good quality, all 9 AA's) |
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What are the exercise recommendations for diabetics?
Why? |
150 min/week
Exercise-sensitive GLUT4 Improves insulin sensitivity (unknown mxn.) Reduce cardiovascular risk Weight loss (T2DM- obesity link) |
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If a patient with Type 2 diabetes comes to you for advice regarding weight loss, what do you suggest?
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- It helps! Even modest loss reduces insulin resistance
- CALORIC RESTRICTION (not nutritional content) - Incorporate physical activity (helps with CV health as well) |
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What happens to Beta cell function over time in Patients with T2DM?
What about in T1DM? |
T2DM- declining B-cell function over time. Insulin secretion deteriorates.
T1DM- B-cells have been damaged early on (autoimmune). No insulin produced. |
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List the major microvascular and macrovascular complication of Diabetes?
Which of the two types of vascular complications can kill the patient? |
Microvascular: retinopathy, neuropathy, nephropathy
Macrovascular: stroke, MI, peripheral vascular disease *these can kill the patient |
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What is the best diagnostic tool if you suspect diabetic retinopathy?
What are the different manifestations of the disease (just list signs)? |
Best tool= dilated eye exam (because sometimes pts are asymptomatic).
Signs: venous bleeding, microaneurysms, hemorrhage, cotton-wool spots, neovascularization, exudates and edema |
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What is the most efficacious treatment in preventing loss of vision in the typical patient with diabetic retinopathy (not complicated eye disease)?
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Laser photocoagulation (decreases oxygen need to eye so it does not participate in as much neovascularization).
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How often should T1DM pts and T2DM pts get screened for their eyes? How about their kidney function?
Why the difference? |
T1DM: 5 years after diagnosis and then once every year
T2DM: immediately and once every year therafter *difference is because we assume T2DM patients had a period of undiagnosed hyperglycemia before diagnosis. |
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What are the 4 major clinical manifestations of diabetic neuropathy? (list them)
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1. Distal sensorimotor polyneuropathy (stocking to glove)
2. Autonomic neuropathy 3. Polyradiculopathy 4. Mononeuropathy/ Mononeuropathy multiplex |
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What is the clinical presentation of diabetic patients with Distal Sensorimotor polyneuropathy?
What about autonomic neuropathy? |
Distal sensorimotor= slow progressive loss of sensation starting from toe upwards (stocking-glove distribution). Affects longest axons first.
Autonomic: orthostatic hypotension, hypoglycemic unawareness, bladder and GU dysfunction |
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What is polyradiculopathy?
How might Mononeuropathy present in a diabetic patient? |
Polyradiculopathy= weakness in the distribution of more than 1 nerve root (one leg, thoracic nerve roots, etc.)
Mononeuropathy= single cranial nerve defect (especially Extroccular nerves), median nerve (mimic's carpal tunnel), etc. |
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What surveillance technique is used to estimate degree of neuropathy in the diabetic patient?
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1. Monofilament test (assess sensation as well as risk for getting food ulcer).
2. Pedal pulses (circulation to leg) 3. ABI (ankel brachial index, claudication). 4. Sensation using tuning for, pinprick, ankle reflex, etc. |
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What counseling should be done regarding foot care in patients with diabetic neuropathy?
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Important!
- wash and check feet daily - use adequate shoes and socks - trim toenails (no fungal infection!) - don't go barefoot, don't cut cuticles |
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What is Charcot's foot?
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Aka. Diabetic Neuropathic Arthropathy
- chronic, progressive, destructive arthropathy (from neuropathy, stress fracture, poor blood flow to area). - joint deforms over time. |
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What is the natural history of Nephropathy in a patient with diabetes over time?
How is this measured? |
Over time patient develops thickening of basement membrane of glomerulus (glomerular sclerosis).
This affects filtration and protein is filtered out. Check microalbumin levels in urine. |
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What screening and what surveillance strategy should you use to assess patients with Diabetic nephropathy?
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Urine albumin/ creatinine ratio (microalbumin test)
*can also do GFR, urinanalysis, BUN, ultrasound and rarely kidney biopsy |
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T or F
The risk of death from CAD (coronary artery disease) in a patient with diabetes and no history of an MI is the same as that of a person without diabetes who has had a previous MI. |
True!
It's scary, but it's true. Macrovascular complications lead to increased risk of MI. |
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What is the main, one word, pathogenic cause of all diabetic complications?
Describe how AGE can cause vascular dysfunction. |
Hyperglycemia
AGE= advanced glycosylation end products. They're reactive derivatives from protein glycosylation rxns. Interact with surface receptor (RAGE) and active cell signaling cascade (Nf-kb, VEGF, etc.) that are proinflammatory, prothrombotic, and make uncontrolled, friable blood vessels. |
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How does the Polyol Pathway (i.e. Aldose reductase pathway) participate in the pathogenesis of diabetic vascular disease?
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Glucose is broken down by ALDOSE REDUCTASE to sorbitol and then fructose. In the process it consumes NADPH which buffers ROS. Increases ROS.
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How doe Oxidative stress contribute to the pathogenesis of Diabetic complications?
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Superactive anions interact with other proteins causing
- increased vascular permeability - damage DNA - increased AGE - activate leukocytes (inflammation) - activates PKC pathway |
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What is the role of the Diacylglycerol-PKC Pathway in the pathogenesis of diabetic vascular disease?
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Hyperglycemia leads to PKC and DAG increase -->
1. VEGF (angiogenesis) 2. collagen, fibronectin, fibrinolysis (capillary occlusion) 3. NFkB- proinflammatory 4. ROS (multiple deleterious effects) |
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What is the role of Aldose Reductase in diabetes management? Are they effective therapy?
What compounds can inhibit AGEs? Is it an effect therapy? |
Various AR inhibitors beneficial in rodents, but clincal trials have mainly negative effect. May play role in neuropathy. (block aldose reductase and thus protect NADPH that helps buffer free radicals).
Aminoguanide inhibit AGE. In human trials, some benefits in treating retinopathy but caused adverse effects. |
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What is the role of antioxidant therapy in reducing diabetic vascular complications?
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Antioxidants (vit C, E, lipoic acid)- not successful in treating diabetic complications in long term human trials
- NADPH oxidase inhibitors - Benfotiamine- compound that decreases oxidative stress. --> effective in animals |
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What is Ruboxistaurin? What is it's role in human diabetic vascular complication prevention?
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It's a PKCB inhibitor (prevents PKC activation and all the downstream proinflammatory, coagulative side effects).
Does not prevent retinopathy, but a pilot study did show reduction in albuminuria. Need more large prospective studies! |
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How do Renin- Angiotensinogen Blockades work?
Has it helped in the treatment of diabetic vascular complications? |
ACE inhibitors (block angiotensin converting enzyme).
ARB- angiotensin receptor blockade. * HAVE ACTUAL EFFECTS on vascular compliance, morbidity, and mortality and therapeutic benefits in microvascular complications! USE IT! |
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What might make a non-diabetic person have a falsely High Hb A1C?
What might make a non diabetic patient have a falsely low Hb A1C? |
A1C dependent on RBC life cycle
High A1C- if RBC lives longer (folate, iron deficiency, etc.) Low A1C- if RBC is cleared faster (hemolytic anemia, etc). |
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In what format should you present A1C levels to patients?
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You should use an equation to calculate "Estimated Average Glucose". This helps the patients put it into perspective (since they're used to getting glucose levels).
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What two large-scale diabetes studies addressed the issue of Glycemic control and Micro Vascular Complication in Type 1 diabetics?
What two trials looked at the same in Type 2 diabetics? |
Type 1: DCCT, EDIC
Type 2: UKPDS, VADT |
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What was the conclusion of the EDIC trial?
Explain the concept of "metabolic memory". |
EDIC (type 1 microvascular complications)
Intensive group and Conventional group by year 11 had minimal difference in A1C. Despite this, intensive group had LOWER incidence of Retinopathy progression, Microalbuminuria, and Neuropathy sxs. Metabolic memory: Period of sustained glycemic control can prevent development of microvascular complications EVEN when control is bad later on. |
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Which Type 2 diabetes trial looked at newly diagnosed patients? Which looked at people who had long standing diabetes?
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UKPDS- newly diagnosed patients
VADT (vetran's affairs diabetes trial)- long standing diabetes, only followed for 5 years |
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What is the conclusion regarding glycemic control and the risks of microvascular complications in patients with Type 2 Diabetes (UKPDS VADT)?
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Improved glycemic control improves risk of microvascular complications (particularly Retinopathy and Nephropathy)
- Also appears to be "metabolic memory" |
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What trials looked at the effects of glycemic control on MACROVASCULAR disease in:
T1DM? T2DM? |
Type 1: EDIC
Type 2: ACCORD, ADVANCE, VADT, Meta-analyses |
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Summarize the role of glycemic control for the prevention of macrovascular disease in Type 1 diabetics?
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Intensive insulin therapy decreases CV events (both fatal and nonfatal) in type 1 diabetics.
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What is the role of HbA1C levels in newly diagnosed T2DM patients?
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It seems to have long-term benefits
- no significant benefit of INTENSIVE therapy however - set higher glycemic targets for older patients and those with comorbidies |
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What lifestyle changes (as indicated by long term studies) delay the progression of diabetic retinopathy, nephropathy, and neuropathy?
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- Smoking cessation
- Aspirin (lower risk of MI, stroke, etc.) - Blood pressure control (put on ACE inhibitors if at all possible) - Treat dyslipidemia (LDL <100) |
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What is the leading cause of visual loss in US adults over the age of 30?
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Diabetes
>10% develop visual loss within 15 yrs of diagnosis. 8% of blindness in US is due to diabetes! |
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What two cell types make up retinal capillaries?
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1. endothelial cells (line capillaries)
2. Pericytes (they cover part of capillary. |
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A HbA1c of what value will lead to increased risk of retinopathy and kidney disease in diabetics?
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>7%
6% or less is normal |
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Why is glycosylated hemoglobin such a problem for diabetics?
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It has a higher affinity for O2 than HbA and causes tissue hypoxia.
Hypoxia and HbA1C itself stimulate VEGF and you get neo-vascularization (but more friable, fragile blood vessels form) and can bleed. |
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How does the incidence of Diabetic Retinopathy differ between Type 1 and Type 2 diabetics?
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Type 1- rare in first 3 years, but after 20 years 99% develop retinopathy. More proliferative disease.
Type 2- up to 23% can get it in the first 3 years, but only about 60% have it after 20 years. Less proliferative disease. |
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What things are you looking for in the funduscopic exam that indicate NONPROLIFERATIVE retinopathy (in diabetics)?
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- Microaneurysms (little pouches in capillaries)
- Ischemia - Exudates (proteins) - Macular edema *no new blood vessels! |
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What signs seen on a fundascopic exam might indicate Proliferative Retinopathy in the diabetic patient?
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- Neovascularization (fragile, abnormal vessels!)
- Hemorrhage - Tractional retinal detachment (from scar tissue formation and fibrosis pulling at retina). |
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What is the best treatment for diabetic retinopathy?
Even before you administer this treatment, what should you do? |
1st- always get blood sugar under control!
2nd- Laser treatment= reduces peripheral oxygen demand for retina. Reduces stimulus to form new blood vessel. |
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Why might a patient with uncontrolled diabetes present with cranial nerve findings?
What is the classic sign in Oculomotor nerve palsy? |
Mononeuropathies (supplied by small blood vessels).
CNIII- controls all but lateral rectus, so eye moves down and out. *Usually pupil is not affected! |
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What is a particularly lethal fungal disease that occurs in patients with uncontrolled diabetes (ex: diabetic ketoacidosis)?
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Mucormycosis
- it starts in the sinuses and spreads into the orbit - it invades vessels and results in thrombosis and blocks off vessels (black eschar= necrotic tissue). |
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Why is advanced mucormycosis nearly impossible to treat and might involve removal of the eye?
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The fungus invades the blood vessels and as such, it causes occlusion. This along with the fact that there's already poor blood flow in diabetic patients makes it hard for IV antifungal to get through.
Pts. need surgery and debridement. |
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What are the 3 classic presentations in someone with grave's disease?
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- Diffuse toxic goiter
- Exophthalmos - Pretibial myxedema |
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T or F
Thyroid eye disease has nothing to do with level of Thyroid hormones (T3, T4). |
True!
It's actually an AUTOIMMUNE disease of antibodies binding to TSH receptor. These can be activating or inactivating (less common). They can cross react with orbital fibroblasts etc. causing an inflammatory response. |
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How is it that the eye in thyroid disease "pops out"?
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1. T&B lymphocytes stimulate fibroblasts
2. they make collagen & GAGs (glycosamino glycans) 3. This infiltrates the muscle and fat of eye and pushes it forward. |
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Explain how 20% of people with thyroid eye disease can have normal thyroid function?
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Thyroid hormone levels/ function does not affect eye findings. These individuals may have antibodies that cause the eye findings but can be euthyroid because T3/T4 levels are normal.
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What are the various presentations of thyroid eye disease (beside exophthalmos/proptosis)?
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- lid retraction
- chemosis (swelling of conjunctiva) - eyelid edema - diplopia- loss of conjugate gaze - optic nerve compression (if muscles get large enough) |
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Which orbital eye muscle is most commonly involved in thyroid eye disease? What would the clinical presentation be in these patients?
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Inferior rectus- it pulls the eyes down in these patients
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What is Rundle's curve?
Define the treatments for each phase. |
It describes the natural history of thyroid eye disease-
1. Active phase- symptoms worsen till they get to a peak. TREAT with lubrication and/or steroids or radiation (severe case). 2. Chronic phase: Fibrosis, muscle enlargement and collagen deposition. Treatment = Surgery |
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Which type of pituitary tumor do you think typically is found by the ophthalmologist: functional or non functional? why?
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Nonfunctional- these get big enough on average to compress chiasm and present with visual loss as first symptom.
Functional tumors are smaller and diagnosed b/c of systemic manifestations. |
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What is the typical visual field deficit seen in patients with a discrete, pituitary adenoma squishing the middle of the optic chiasm?
What will happen to their visual acuity? |
Bitemporal hemianopsia (temporal visual field loss on both eyes)
Visual acuity is good (macula is still working) |
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Anterior chiasmal lesion on the right side will cause....?
Posterior chiasmal lesion on Right side will cause...? |
Anterior- total loss in R eye.
Posterior- left side of each eye is lost. |
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What is a junctional scotoma and what visual field loss would you expect?
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Some inferior nasal fibers can bulge forward into optic nerve space. A correctly placed lesion can give a loss in both a temporal field and superior field causing a "pie in the sky" look.
*note it respects the midline (because only fibers from one side affected |
