Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
118 Cards in this Set
- Front
- Back
|
diabetes ass with hla-dr3 or hla-dr4 |
type 1 |
|
|
diagnose dm |
randome plasma glucose >200 WITH polyuria, polydipsia and weight loss fasting (8hours) >126 on 2 seperate occasion OGTT >200 2 hours post prandial (rarely used |
|
|
causes of increase BUN |
waste products protein breakdown GI bleed high protein low carb diet |
|
|
normal ha1c |
5.5-7% |
|
|
ha1c tells you what |
pts glucose control ver the past 2-3 months/ 8-12 weeks |
|
|
what diagnostic of impaired glucose tolerance |
FBG >100 <125
|
|
|
normla fasting glucose? |
60-99 |
|
|
total carb intake should e |
55-60% |
|
|
total fat intake shuld be |
20-30% |
|
|
TOTAL FIBER INTAKE SHOULD BE |
25G/1000 CALOries |
|
|
total protin should be |
10-20% |
|
|
your pt has ketones what should be treatment |
insul;in |
|
|
if h1a is too low |
than therapy is too intense |
|
|
what is the rule for insulin thepay |
0.5u/kg/day give 2/3 in the moniign and the reminign 1/3 in the evening |
|
|
describe conventional split dose mixture |
morning dose of insulin is 2/3 NPH and 1/3 regular evenig dose is 1/2 NPH and 1/2 regular |
|
|
describe intensive therapy |
reduce or omit th enight dose and add a portion at bedtime |
|
|
insulin analogs |
aspart ( novolog) Glargine (lantus) long listpro (humalog) fast |
|
|
somogy |
"rebound" nocturnal hypoglycemia develops stimulates counter regulatory homrones which causes b.s to be raised when you wake pt up at 3am they are hypoglycemic and repounds at 7am elevated b.s |
|
|
treatment of somogy |
reduce/ omit bedtime dose of insulin |
|
|
dawn phenomena |
tissue become desensitized to insulin nocturnally b.s becomes progressivly elevated trhoughout the night = in elevated blood glucose at 7 am |
|
|
treat dawn phenamena |
add or increase the at-bedtime dose of insulin |
|
|
syndrome x |
htn obesity and abnormal lipid profile (low hdl, high triglycerides) |
|
|
metabolic syndrome |
waste >40 men >35 women bp >130/85 triglycerides >150 FBG >100 HDL <40 men and <50 women |
|
|
how to diagnose metabolic syndrome |
has to have 3 of the 5 criteria
|
|
|
metaboic syndorme? whats the risk? |
risk of diabetes is high but risk for sudden cardioembolic death is hihg they are ligkly to rop dead |
|
|
vaginits/ frequent vaginits shoudl be concerned for? |
type 2 dm |
|
|
pt who comes in frequently for skin infection |
type 2 dm |
|
|
pts with type 2 dm often present with these symptoms |
insidious asymtpomatic 3Ps recurrent vagiitis peripehral neuropahty blurred vision chronic skin infections |
|
|
stimulates pancreas to release mroe insulin |
sunfonyureas |
|
|
2nd gfeneration sulfonyureas |
glyburide, glipizide, gimeperide |
|
|
good adjunt to sunfonyureas |
biguanide |
|
|
standard of caare with initial diagnosnis of type 2 dm |
biguanide |
|
|
side effect of biguanide |
lactic acidosis |
|
|
how will pt preesent with sde effect of biguanide |
muslce pain ( difficult if they are n a statin) |
|
|
bind to disaccaride more readily than sucrose so less glucose is absorbed in gut |
alpha glucosidase inhibitor |
|
|
alpha glucosidase inhibitro drugs |
acarbose miglitol |
|
|
thiazolidiniones how deos it work |
decrease gluconeogeneis decrease production of glucose |
|
|
drugs that are thiazolidinodens |
avandia (rosiglitazone) and actos (pioglitazone |
|
|
majpr side effect of tzd |
headrt failure |
|
|
which pts do we avoid giving tzd in |
heart failure |
|
|
both dka and hhks have what features |
state of intracellular dehydration |
|
|
signs of dka |
acute! 3Ps weakness fatigue n/v kussmaul breathing altered loc fruity breath orthostatic hypotension with tcycardia (dehdyrated) poor skin turger ( dehdyrated) |
|
|
how high does dka pts bs go? |
350 maybe the msot, not as high as hhnk (1200) |
|
|
realtion with pH and k |
low pH causes hyperkalemia because hydrogen oins go into the cell and k comes out |
|
|
normal serum osmol |
275-290 roughly 280 should be bout 2 x Na |
|
|
know the fluid status of the patietn what do you order |
serum osmol |
|
|
what kind of fluids hydrate the cells |
hypootonic fluids |
|
|
labs of dka |
bs >250 ketonemia ketonuria glycosuria acidosis <7.3 low hco3 low pCO2 elevated hct elevated bun/creat hyperkaemai leukocytosis hyperosmolality |
|
|
treament of dka |
protect airway o2 isotonic first 1 l in 1 hr than 500 if bs >500 use 1/2 ns afte rfirs thour whsn bs <250 change to d51/2 insulin drip correct acodisos if pH < 7.1 wicarb drip don treat hyperkalmenia strict I+O suppportive |
|
|
how to dose an insulin drip for dka |
0.1u/kg iv bolus f/b 0.1 u/kg/hr if bs doesnt fall by atleast 10% repeat bolus |
|
|
sigs of hhnk |
polyuria weak change inloc hypotension tacycardia poor skin turgor signs of dehydration |
|
|
labs of hhnk |
greatly elevated glucose >600 usually >1000 hyperosmolor >310 elevated bun/creat elevated ha1c normal pH normal anion gap |
|
|
treat hhnk |
ns after hemodynamic stable or Na over 145 change to 1/2 ns about 4-6l in first 8-10 hrs when bs is 250 add dextrose to solution 15u reg insulin iv f/b 10-15u sq immediatly supportive care |
|
|
insulin drip in controversial in which dm |
2 hhnk consult endocrinologist |
|
|
common presentation of hyperthyroidism |
graves disease |
|
|
common presentaiton of hypothyoidism |
hashimotos thyroiditis |
|
|
etiology of hyerthryoirdism |
women 20-40 graves disease toxic adenoma, subacute thyroidiits, tsh secreting tumor of th pituitary and high dose amioderone |
|
|
etiology of hypothyroidism |
primary disease of thyroid gland pituitary deficiency of tsh hypothalamic deficiency of trh iodine deficiency hashimoto idiopathic damage to gland |
|
|
signs of hyperthyroidism |
nervous anxiety increase sweating fatigeu emotionl lability fine tremots hyperreflexic dtr increased appetitie weight loss smooth warm moist velvety skin fine thin hair exopthalamos lid lag tacy cardia heat intolerance |
|
|
signs of hypothyroidism |
weakness muscle fatigue arthalgia cramps cold intol consitpation weight gain dry skin hair loss brittle nails puffy eyes edema of hands and feet bradycardia slow dtr hypoactive bowel sounds |
|
|
labs for hyer thyroidsism |
tsk t3 t4 thyroid resin uptake and free thyroxin index t3 lways elevate because soemtimes t4 is normal ana elevated w/o evidence of lupus or collagen disease radioactive iodine uptake nd scan to establish etiology mri of orbits for vizualizing graves |
|
|
most sensitie test in hypo/hyperthryodis |
tsh |
|
|
radioactive iodine uptake result in hyperthyroidism |
high iodine uptake is consistant with graves disease low uptake is consistant with subacute thryoiditis |
|
|
visualize graves opthalmopathy |
mri |
|
|
labs for hypothryoidism |
elevated tsh low - low normal t4 resin t3 uptake - decreased - t3 is not realibel inthis hyponatremia hypoglycemia |
|
|
t3 is not realible in which disease |
hypothyroidism |
|
|
hyponatremia and hypoglycemia is seen in which thyroid disorder |
hypothyroidism |
|
|
manage hyperthyroidism |
referal propranolol begin at 10mg po-80mg qid thiourea for mild cases, small goiter or fear of isotopes methimazole (tapazole) 30-60 every day in 3 divided doses ptu 300-600 in 4 dividied doses radioactive iodine 131 to destroy goiters thyroid surgury ( must be euthyroid before) lugols solution 2-3 gtt po daily for 10 days to reduce vascularity of the gland |
|
|
pts with subacute thyroidiitis are treated with |
propranolol |
|
|
lugols solutions for what |
2-3 drops a day for 10 days to redues vascualroty of the gland |
|
|
drugs for hyperthryoidism |
thioureas mithamazole (tapazole) 30-60 daily in 3 divided doses ptu 300-600 daily in 4 divided dosases radioactive ioding lugos solution propranolol |
|
|
management of hypothyroidism |
levothyroixine 50-100mcg daily increase by 25mcg until symptoms stbaalize >60 yrs decrease dosage |
|
|
treatement of thyroid crisis |
ptu - 150-250 q6 or methimazole 15-25 every 6 hours WITH the follwoing within 1 hour: lugols solutio 10gtt tid OR sodium iodide 1gm slow iv with propranolol 0.5-2 gm iv q4/ 20-120mg po q6 with hydrocortisone 50 q6 with reductiona s situation improves |
|
|
which meds to avoid during a thyroid crisis |
asa |
|
|
treatment of myxedema coma |
airway fluid replacement synthroid 400mcg iv x1 thn 100 mcg iv eery day support hypotension slow rewarming with blankets NOT HYPERTHERMIA BLANKETS avoid circulartory collapse symptomatic care |
|
|
high dose of amioderone can cause |
hyperthryoidism |
|
|
first test to order in thyroid issues |
tsh |
|
|
this an exacerbate a thyroid storm |
aspirin so take tylenol |
|
|
cause of c cushing's disease |
acth hyper secretion by the pituitary adrenal tumors Chronic administration of glucocorticoids |
|
|
Signs and symptoms of C Cushing syndrome
|
Central obesity
Moon face Acne Poor wound healing Purple striae hirsutism Hypertension Weakness Amenorrhea Impotence Headache Polyurea And thirst Labile mood Frequent infections |
|
|
Laboratory findings of Cushing's syndrome
|
Hyperglycemia
Hypernatremia Hypokalemia Glucosuria Leukocytosis Elevated plasma cortisol in the morning Hypertension Dexamethasone suppression test to differentiate cause Serum ACTH |
|
|
What will help differentiate the cause of Christians and Addison's disease
|
Dexamethasone suppression test
|
|
|
Management of Cushing's disease
|
Depending on the cars you will have to: Discontinue medications that are causing symptoms
Transphenoid resection of pituitary adenoma Surgical removal of the adrenal tumors Resection of ACTH secreting tumors Manage electrolyte imbalance |
|
|
Causes of Addison's disease
|
Deficient cortisole androgen and aldosterone
Auto immune destruction of adrenal glands Metastatic cancer Bilateral a genome hemorrhage with anticoagulant therapy Pituitary failure resulting in decreased ACTH |
|
|
Signs and symptoms of Addison's disease
|
Hyperpigmentation in buccal mucosa and skin creases especially knuckles nailbeds nipples Palmer creases and posterior neck
Diffuse tanning and freckles Orthostasis and hypotension Scant axillary and pubic hair Rapid worsening of chronic signs and symptoms in the acute phase Fever in the acute phase Changes in level of consciousness in the acute phase |
|
|
Laboratory findings in Addison's disease
|
Hypoglycemia
Hyponatremia Hyperkalemia Hypotension Elevated ESR Lymphocytosis Plasma cortisone less than five at 8 AM |
|
|
Management of Addison's disease in the outpatient
|
Specialist
Glucocorticoids and mineralocorticoid replacement Glucocorticoid replacement with hydrocortisone Mineralocorticoid replacement with Florinef / fludrocortisone acetate |
|
|
Management of Addison's disease inpatient
|
Hydrocortisone (solu-cortef) 100 to 300 mg IV initially with normal saline
Replace volume with D5 normal saline at 500 ml per hour for four hours and then taper per condition Vasopressin or a's are usually ineffective treat the underlying causes which is usually infection |
|
|
What is another name for ACTH test
|
cosynotrphyn test |
|
|
In the acute phase of Addison's disease what are some signs and symptoms you may see
|
Rapid worsening of chronic signs and symptoms
Fever Change of level of consciousness |
|
|
Causes of SIADH
|
Release of ADH occurs independent of osmolality or volume dependent stimulation
Inappropriate water retention Tumors production of ADH Skull fracture or head trauma CNS disorder Chronic lung disease |
|
|
Signs and symptoms of SIADH
|
Neurologic changes because of the hyponatremia anywhere from mild headache to seizures or coma
Decrease DTR Hypothermia Weight gain or eDema Nausea vomiting Cold intolerance |
|
|
Laboratory findings in SIADH
|
Hyponatremia yet euvolemic
Decrease serum osmolality < 280 Increase urine osmolality> 100 Urine sodium greater than 20 Renal cardiac thyroid functions are all normal |
|
|
Causes of central diabetes insipidus
|
Idiopathic causes Damage to hypothalamus or pituitary Surgical damage Accidental trauma Infection Metastatic carcinoma |
|
|
what Central diabetes insipidus |
Related to pituitary or hypothalamus damage resulting in ADH deficiency |
|
|
What is nephrogenic diabetes insipidus
|
Due to a defect in the renal tubules resulting in renal insensitivity to ADH
|
|
|
Causes of nephrogenic diabetes insipidus
|
Familial X trait
Acquired from pyelonephritis, potassium depletion, sickle cell anemia, chronic hypercalcemia, medications like lithium |
|
|
Signs and symptoms of diabetes insipidus
|
Thirst craving for water
Fluid intake 5 to 20 L perday Polyurea 2 to 20 L per day Nocturia Weight loss fatigue Changes in level of consciousness Dizziness Elevated temperature Tachycardia hypotension Poor skin turgor dry mucous membranes |
|
|
Lab findings in diabetes insipidus
|
Hypernatremia
Elevated B UN and creatinine Serum osmolality greater than 290 urine osmolality less than 100 Urine specific gravity low less than 1.005 |
|
|
If central diabetes insipid as is suspected what do you do
|
Vasopressin challenge test
|
|
|
So What is the vasopressin challenge test
|
0.05-0.1 ML nasally or 1 µg sub Q or Iv and measure urine volume test is positive in central diabetes insipidus and negative in nephotogenic diabetes insipid us If there's no apparent cause do an MRI to look for masses or lesions |
|
|
Treatment of SIADH
|
Cheat the underlying cause
If sodium is greater than 120 restrict fluids to 1 L per day If sodium Is between 110 and 120 without any neurologic symptoms the strict fluids to 500 ML's pretty If serum sodium is less than 110 or new logic symptoms are present replace with iso tonic or hypertonic saline and Lasix at 1-2 meq/h Monitor sodium and potassium losses hourly and replace |
|
|
Treatment of diabetes insipidus
|
If serum sodium is greater than 150 given D5W to replace half the volume deficit in 12 to 24 hours rapid lowering of sodium can cause cerebral edema
If sodium is less than 150 substitute half normal saline or normal saline ddavp 1-4 micrograms IV or subq every 12 to 24 hours for acute situations Maintain dose of DDAVP at 10 µg every 12 to 24 hours intranasally |
|
|
What is pheochromocytoma
|
Rare but serious disease resulting from excess catecholamine release characterized by peroxisomal or sustained hypertension always do to a tumor of adrenal medulla
|
|
|
Signs and symptoms of pheochromocytoma
|
Hypertension labile
Top diaphoresis Hyperglycemia Severe headaches Palpitations Profuse sweating Tremor Tachycardia Weight loss Postural hypotension |
|
|
Of the signs and symptoms related to pheochromocytoma which are not related to thyroid function
|
Postural hypotension and hyper tension labile
|
|
|
If you want to differentiate between pheochromocytoma and thyroid function what should you do
|
The Depression management check for hypertension and postural hypotension
|
|
|
Number one lab to test four in pheochromocytoma
|
TSH to rule out thyroid problems
|
|
|
Laboratory findings in pheochromocytoma
|
Plasma free metanephrines
Plasma concentration of normetanephrine greater than 2.5 or metanephrine levels greater than 1.4 Assay of urine catecholamines which include total and fractionated metanephrines vanillylmandelic acid VMA and creatinine to this for 24 hours greater than 2.2 µg metanephrines per milligram of creatinine ants greater than 5.5 µg VMA per milligram of creatinine CT of adrenals used to confirm and localized tumor |
|
|
Management of pheochromocytoma
|
Surgery is treatment a choice
Alpha adrenergic medications preoperatively : phetolamine (regitine) 1-2mg iv q5 min until controlled then 1 to 5 mg IV every 12 to 24 hours As soon as possible converts a PO phenoxybenzamine (dibenzyline) |
|
|
What's the monitor for postoperatively after pheochromocytoma
|
Hypotension because of the pleated catecholaminesAdrenal insufficiencyHemorrhage
|
|
|
Send in symptoms of hypoglycemia |
Headache hunger difficulty with problem-solving sweating shaking tremor anxiety irritable behavior changes it can progress Ta coma and seizures without treatment
|
|
|
A cute adrenal insufficiency is precipitated by
|
Surgery
Infection Exacerbation of comorbid illness Sudden withdrawal of long-term Golucocorticoids |
|
|
Hyperglycemia and type I diabetes results from
|
Inability of the glucose to enter the self to be used for energy
|
|
|
Ketoacidosis the Results from
|
The use of free fatty acids for energy
|
|
|
Hemoglobin A-1 C level indicates good control
|
5.5 to 7
|
|
|
Postprandial goal of insulin therapy in diabetics
|
Less than 180
|
|
|
Hemoglobin A-1 C provides glycemic control for how long
|
8 to 12 weeks
|
