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Diabetes & Endocrine Disease Sheets

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Diabetes & Endocrine Disease Sheets
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Buzz Words polyuria ADH deficiency Diabetes Insipidus Hallmark 1. DI is caused by an ADH insufficiency Epidemiology Pathophysiology Cause: Same causes as hypopituitarism (slide 26) Post-surgical is most common Leads to a loss of ADH and thus, inability to concentrate urine and regulate sodium balance in the serum ADH: acts on the distal tubule and collecting duct of the kidney to increase water reabsorption into the serum Lowers hyperosmolarity and raises hypervolemia by thirst mechanism Central: low ADH levels released from pituitary Can be complete or partial Nephrogenic: kidney is unresponsive to ADH Clinical Manifestation/ Clinical Presentation/ Physical Exam Polyuria >3L/nocturia Polydipsia Dehydration Cravings for ice water Children may have enuresis HYPERnatremia (weakness, AMS, seizures) Differential Diagnosis Work Up Lab Tests/ Radiology Urine sample for analysis of concentration Low urine osmolality (can be high with partial DI) High plasma osmolality Fluid deprivation test (use only when plasma Osm normal and pt having hypotonic polyuria) to compare urine and plasma Osm Treatment 1. ADH analog = DDAVP a. Subcutaneous, intranasaly, orally depending on how bad it is, their sxs 2. Start 0.05mg BID (max 0.4mg q8) 3. Assess for improvement in sx = decreased urine output, increased urine osmolality, and decreased thirst 4. When stable dose is found, drink only when
Transcript
Page 1: Diabetes & Endocrine Disease Sheets

Buzz Words polyuria ADH deficiency

Diabetes Insipidus

Hallmark

1. DI is caused by an ADH insufficiencyEpidemiologyPathophysiology Cause:

Same causes as hypopituitarism (slide 26) Post-surgical is most common Leads to a loss of ADH and thus, inability to concentrate urine and

regulate sodium balance in the serum ADH: acts on the distal tubule and collecting duct of the kidney to

increase water reabsorption into the serum Lowers hyperosmolarity and raises hypervolemia by thirst

mechanism Central: low ADH levels released from pituitary Can be complete or partial Nephrogenic: kidney is unresponsive to ADH

Clinical Manifestation/Clinical Presentation/ Physical Exam

Polyuria >3L/nocturia Polydipsia Dehydration Cravings for ice water Children may have enuresis HYPERnatremia (weakness, AMS, seizures)

Differential DiagnosisWork UpLab Tests/ Radiology

Urine sample for analysis of concentration Low urine osmolality (can be high with partial DI) High plasma osmolality Fluid deprivation test (use only when plasma Osm normal and pt

having hypotonic polyuria) to compare urine and plasma Osm

Treatment 1. ADH analog = DDAVPa. Subcutaneous, intranasaly, orally depending on how bad it is,

their sxs2. Start 0.05mg BID (max 0.4mg q8)3. Assess for improvement in sx = decreased urine output, increased urine

osmolality, and decreased thirst 4. When stable dose is found, drink only when thirsty VERY IMPT

Side Effects & ComplicationsHealth MaintenanceMonitoringAnatomy

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Buzz Words Too much

ADHSIADHsyndrome of inappropriate antidireutic hormone secretion

Hallmark 1. Syndrome of inappropriate antidiuretic hormone hypersecretion 2. Most common cause of HYPOnatremia leading to elevated urine

osmolality and low plasma osmolality from excess ADH release 3. Opposite of DI

EpidemiologyPathophysiology Water retention leads to hyponatremia and decreased plasma osmolalityClinical Manifestation/Clinical Presentation/ Physical Exam

no symptomsslow/mildly developing hyponatremiaNO edema

Differential Diagnosis 1. Adrenocortical insufficiency2. Hypovolemic hyponatremia syndromes3. Congestive Heart Failure

Work UpLab Tests/ Radiology

Hyponatremia <125mEq/L (normal is 125-141)Low or low-normal serum concentration of urea and uric acidLow serum osmolalityConcentrated urineElevated circulating vasopressinUrine osmolality of >300nmol/kg

Treatment 1. Treat with water restriction FIRST2. Replace Na3. Demeclocycline 600-1200mg bid-qid or Lithium carbonate 600-

1200mg bid-qid4. High Na diet

Side Effects & ComplicationsHealth MaintenanceMonitoringAnatomyImages

Page 4: Diabetes & Endocrine Disease Sheets

Buzz Words Hypoglycemia

Hallmark

1. A blood glucose of <80mg/dLEpidemiologyPathophysiology Insulin

Oral Agents (Most will need admission)Other

Clinical Manifestation/Clinical Presentation/ Physical Exam

ShakyBlurred Vision HANauseaConfusionSeizureComaDeath

Differential DiagnosisWork UpLab Tests/ RadiologyTreatment If they took insulin and forgot to eat:

1. Sugar (oral)2. Glucagon if unable to establish IV3. Dextrose IV (D50 25grams)4. FOOD!!!!5. LOOK for Underlying Cause6. Education

IF DUE TO ORAL AGENTS1. Usually Require Admit, Consider Octreotide 2. Re-Check FSBG Before Discharge

If overdose:1. Antidote: IV Glucagon

Side Effects & Complications Beta Blocker Mask Symptoms of HypoglycemiaBarbiturates, Salicylates, EtOH, Renal Insufficiency, Malnutrition.

Health MaintenanceMonitoringAnatomyImages

Buzz Words Type 2 DM

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Hallmark Insulin resistanceNew Onset:Non-Compliance:Abnormally High: DKA:HHS:

EpidemiologyPathophysiology New Onset: poor diets, overweight

Non-Compliance: high glucose at baselineAbnormally High: infection, alcoholDKA:HHS:

Clinical Manifestation/Clinical Presentation/ Physical Exam

New Onset:fatigue, polyuria, polydipsia, overweight, unexplained opportunistic infsNon-Compliance:

Abnormally High:

DKA:

HHS:Differential DiagnosisWork UpLab Tests/ Radiology

New Onset:Non-Compliance:Abnormally High: look for cause- infection, CBC, Urinalysis, Chest XrayDKA:HHS:

Treatment New Onset DM:1. Hydration 2. Glucotrol (glipizide), Glucagon3. Follow up

Non-Compliance:1. Make sure they are not DKA2. IV Fluids3. Education, Follow up

Abnormally High:1. IV Fluids

Side Effects & ComplicationsHealth MaintenanceMonitoringAnatomyImages

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Buzz Words Diabetic Ketoacidosis

Hallmark Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Ketones in the bloodAcidosis

Epidemiology DKA occurs mostly in type 1 diabetes. Mortality 1-10%

Pathophysiology Insulin deficiency causes the body to metabolize triglycerides and muscle instead of glucose for energySerum levels of glycerol and free fatty acids (FFAs) rise because of unrestrained lipolysis, as does alanine from muscle catabolism. Hyperglycemia caused by insulin deficiency produces an osmotic diuresis that leads to marked urinary losses of water and electrolytes

• Potassium and Sodium– HOWEVER SERUM POTASSIUM

MAY BE ELEVATED

Clinical Manifestation/Clinical Presentation/ Physical Exam

nauseavomiting abdominal pain high blood glucose: high meter reading at homeUsually blood glucose is >250If meter says high it is >500

Differential DiagnosisWork UpLab Tests/ Radiology

DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. BMP, CBC if glucose is >250A-B-CLook for underlying causes such as infection, MI: CIP (cardiac injury profile), CXR- look for pneumonia, UA- look for ketones in urineCBC- looking for infectionBMP (anion gap): Na, Cl, K, CO2, BUN, CrSerum KetonesArterial Blood Gas (pH < 7.35)UA (+glucose, +ketones)

Treatment Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia

Side Effects & Complications can progress to cerebral edema, coma, and death.Health MaintenanceMonitoringAnatomy

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Buzz Words Hyperosmolar Hyperglycemic StateHHS (HHNK)

Hallmark

Epidemiology High Mortality Rate It most often occurs in type 2 DM, often in the setting of physiologic stress.

PathophysiologyClinical Manifestation/Clinical Presentation/ Physical Exam

fluid deficitspolyuriano ketones in urine

Differential DiagnosisWork UpLab Tests/ Radiology

Nonketotic hyperosmolar syndrome (NKHS) is a metabolic complication of diabetes mellitus (DM) characterized by: hyperglycemia, extreme dehydration, hyperosmolar plasma, and altered consciousness.NKHS is diagnosed by severe hyperglycemia and serum hyperosmolarity and absence of significant ketosis.

Treatment Treatment is IV normal saline (10Liter average deficit), insulin, monitor & correct K+, evaluate for underlying causeIn ICU

Side Effects & Complications Complications include coma, seizures, and death

Health MaintenanceMonitoringAnatomyImages

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Buzz Words Alcoholic Ketoacidosis

Hallmark

EpidemiologyPathophysiologyClinical Manifestation/Clinical Presentation/ Physical Exam

• Read this on your own2-3 days after stopping EtOHAnion gap metabolic acidosisUrine and Serum Ketones

Differential DiagnosisWork UpLab Tests/ RadiologyTreatment Treatment: IV Normal Saline, Thiamine, D50

Side Effects & ComplicationsHealth MaintenanceMonitoringAnatomyImages

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Buzz Words Hyperthyroid Hallmark

EpidemiologyPathophysiologyClinical Manifestation/Clinical Presentation/ Physical Exam

shakyweight loss, thin buildheat/cold intolerancethin hairbaseline tachycardiaproximal muscle weaknessatropy of eye muscles, looked pushed forward

Differential DiagnosisWork UpLab Tests/ Radiology

TSH, T3, Free T4, EKG

Treatment Beta Blocker tp fix the sxsAlbalte thyroid medications take out

Pharmacologic therapyPropylthiouracil (PTU )

150-600 mg/d, 3-4/d Inhibit synthesis and T4-T3 conversion Rash,urticaria, and abnormal taste Agranulocytosis (0.2-0.3%) , hepatic

necrosis,cholestasisMethimazole 10-40 mg/d, single dose Inhibit synthesis Rash, urticaria Agranulocytosis,hepatic necrosis,cholestasis In pregnancy : aplasia cutis, esophageal atresia

Radioiodine therapy Surgery : Thyroidectomy

Side Effects & ComplicationsHealth MaintenanceMonitoringAnatomyImages

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