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Hypoglycemia (1)
- Glucose is the sole energy source for the brain
- Symptoms of hypoglycemia depend on the glucose level and the rate of glucose drop
- Hypoglycemia can mimic stroke, TIA, epilepsy, MS, psychosis, Stokes-Adams
- Counterregulatory hormones (glucagon and epinephrine) cause the release of glycogen from the liver
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FirstRanker.comHypoglycemia (2)
- Sympathomimetic symptoms: sweating, tremor, pallor (vasoconstriction), anxiety, nausea
- Sympathomimetic symptoms can be masked by beta blockers
- Neuroglycopenia symptoms: dizziness, psychosis, confusion, coma
Always consider hypoglycemia in an unresponsive patient – check a rapid blood glucose level
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Hypoglycemia (3)
- Differential diagnosis
- Insulinoma
- Medications / drugs / alcohol
- Extrapancreatic neoplasm
- Hepatic disease (depletion of glycogen stores)
- Deficiency of counterregulatory hormones
- Critically ill, stressed infants, hypothermia
- Dumping syndrome
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- Artifactual
- Continued glycolysis by WBCs in lab tube
- Leukemia, polycythemia
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Hypoglycemia (4)
- Distinguishing excess endogenous insulin from excess exogenous insulin
- Pancreas cleaves proinsulin to insulin plus immunoreactive C-peptide
- Excess endogenous insulin has measurable C-peptide (not so with excess exogenous insulin)
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FirstRanker.comHypoglycemia (5)
- Standard treatment options
- D50
- D25 (peds)
- D10 (neonates)
- Glucagon 1 mg IM/IV (converts liver glycogen to glucose)
- D10 drip if recurrent or overdose
- Hydrocortisone (adrenal insufficiency)
- Octreotide – inhibits insulin secretion and helps prevent rebound hypoglycemia in the setting of glucose infusion treatment of refractory sulfonylurea-induced hypoglycemia
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Oral Agents In Diabetes Treatment (1)
- Two classes: hypoglycemics & antihyperglycemics
- Hypoglycemic agents:
- Sulfonylurea agents
- Chlorpropamide, tolbutamide, acetohexamide tolazamide, glipizide, glyburide, glimepiride
- Stimulate pancreatic insulin secretion
- Cause profound hypoglycemia in overdose
- Long duration of action
- Chlorpropamide also can cause SIADH
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- Repaglinide (Prandin)
- Can also cause hypoglycemia
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- Sulfonylurea agents
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Oral Agents In Diabetes Treatment (2)
- Antihyperglycemic agents
- Less likely to cause hypoglycemia in overdose
- Metformin
- Rarely causes lactic acidosis
- Alpha-glucosidase inhibitors
- Inhibit intestinal hydrolysis of polysacharides
- Oral sucrose will not be absorbed
- Thiazolodenediones (Avandia/Actos)
- Limited overdose experience
- Can worsen CHF
- Other side effects
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- Metformin
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Hypoglycemia Pearls
- Always admit if sulfonylurea overdose
- Most symptomatic in 4 hours (can be delayed)
- Octreotide inhibits insulin secretion
- Give thiamine with glucose in hypoglycemic malnourished patients
- Glucagon may not be effective in chronic alcoholics, those with liver disease or infants with low, liver glycogen stores
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FirstRanker.comDiabetic Ketoacidosis Pathophysiology
- Relative lack of insulin + stressors causes hyperglycemia
- Hyperglycemia-induced osmotic diuresis causes polyuria, dehydration, hypovolemia, electrolyte loss (K, Mg, Phos)
- Switch over to fat breakdown for energy source causes ketonemia (acidosis)
- Metabolic acidosis causes compensatory hyperventilation (Kussmaul respirations)
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Precipitants of DKA
- The "I's" have it!
- Infection (UTI, pneumonia, pancreatitis)
- Infarction (e.g. AMI)
- Infraction (noncompliance)
- IUP (pregnancy)
- Ischemia (CVA)
- Illegal (substance abuse)
- Iatrogenic (drug interactions)
- Idiopathic (new onset DM)
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Fluids / Bicarbonate in DKA
- Initial fluid resuscitation for hypovolemia
- Replace electrolytes (phosphate, potassium)
- Insulin drip (after checking potassium)
- Sodium bicarbonate is rarely indicated
- The hazards of bicarbonate use include
- Paradoxical CSF acidosis
- Decreased oxygen-hemoglobin dissociation (shifts curve to left)
- Overload of sodium
- Hypokalemia, hypophosphatemia
- Cerebral edema in children
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- The hazards of bicarbonate use include
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FirstRanker.comSodium / Phosphate in DKA
- Pseudohyponatremia
- (*Hyperosmolar as opposed to hypoosmolar state)
- Sodium is artifactually ? 1.6mEq/L for every 100 mg/dL ? glucose over 100
Hypophosphatemia is possible: Respiratory depression, muscle weakness CHF, decreased mental status (failure to generate adequate ATP)
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Potassium in DKA
- Serum K+ level may be elevated, normal or low
- Initial hypokalemia indicates massive total body depletion (usual deficit is 3-7 mEq/L)
- Replacement recommendations
- K < 3.3: Hold insulin, give 40 mEq per hour until = 3.3
- K = 3.3 but < 5.0: give 20-30 mEq in each liter IVF to keep K 4-5 mEq/L
- K = 5.0: No replacement but check Q2 hr
- Serum potassium will decline with insulin and correction of acidosis (drives K+ into cells)
- Cardiac arrest in DKA is often 2° to precipitous hypokalemia (insulin therapy, acidosis correction or fluid therapy with increased urinary losses)
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FirstRanker.comComplications of DKA Treatment
- Hypoglycemia due to excess insulin
- Add glucose administration when glucose = 250 mg/dl
- Hypokalemia is associated with insulin administration, bicarbonate, hydration
- Bicarbonate therapy causes CSF acidosis
- Cerebral edema
- Patients at risk: Young, new onset DM
- Controversial: Possibly 2° to over-hydration, rapid osmotic changes, hypoxemia, sodium bicarbonate
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Alcoholic Ketoacidosis (1)
- Binge drinking with heavy alcohol consumption and decreased food intake for several days (starvation ketosis)
- Imbalance of insulin levels and counter-regulatory hormones
- Ethanol metabolism inhibits gluconeogenesis
- Abdominal pain, nausea, vomiting, dehydration, disorientation
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Alcoholic Ketoacidosis (2)
- Alcohol levels are usually low or negative and glucose is often mildly elevated with low bicarbonate and high anion gap
- Urinary ketones may be weakly positive
- Treatment: Glucose + saline (D5NS), thiamine and potassium repletion
The major and earliest ketone produced from fat breakdown is beta-hydroxybutyrate, but the lab-measured ketone is acetoacetate. Therefore, lab tests for ketones may be falsely negative.
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Hyperosmolar Hyperglycemic Non-ketotic State HHNS (1)
- Similar to DKA but has important distinctions
- No ketoacidosis
- Glucose is usually higher, often >1000
- Serum osmolality is often greater than 350
- Most often occurs with NIDDM
- Higher mortality than DKA
- DKA has shorter onset
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- Precipitating factors include
- Infection, especially pneumonia
- Myocardial infarction
- CVA
- GI bleed
- Pyelonephritis
- Pancreatitis
- Uremia
- Subdural hematoma
- Peripheral vascular occlusion
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Hyperosmolar Hyperglycemic Non-ketotic State HHNS (2)
- Common comorbid conditions
- Renal insufficiency
- Vascular disease
- Poor access to water
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- Common associated medications
- Diuretics
- Propranolol
- Corticosteroids
- Calcium channel blockers
- Phenytoin
- Cimetidine
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HHNS is often the initial presentation of NIDDM
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Hyperosmolar Hyperglycemic Non-ketotic State HHNS (3)
- Physical findings
- Dehydration
- Altered sensorium
- Focal neurologic findings (often mistaken for a stroke)
- Coma is rare
- Treatment
- Normal saline
- Average fluid deficit 8-12 liters
- ½ of deficit in first 12 hours, rest over next 24 hours
- Initial 1-2 liter bolus as clinically indicated
- Insulin infusion (usually lower doses than in DKA)
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Cerebral edema possibly 2° to rapid fluid replacement or the severity of the condition
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FirstRanker.comThyroid Hormones
- TRH from hypothalamus stimulates TSH release from anterior pituitary
- TSH stimulates thyroid gland
- Thyroid hormones (T3, [20%] T4 [80%]) are synthesized and released
- Thyroid hormone production depends on iodine intake. Excess iodine blocks hormone release
- T3 is biologically 4x more active than T4
- T3 and T4 provide feedback inhibition of TSH release
- T3 and T4 act on cells
- Increase rate of cell metabolism
- Increase rate of protein synthesis
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Hyperthyroidism (1)
- Causes
- Graves' disease (most common):
- An autoimmune disorder (thyroid-stimulating immunoglobulins mimic the action of TSH)
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- Toxic thyroid adenoma, toxic multi-nodular goiter
- Thyroiditis
- Pituitary adenoma
- Excess iodine in diet
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- Graves' disease (most common):
Goiter
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FirstRanker.comHyperthyroidism (2)
- Signs and symptoms
- Nervousness, tremor, insomnia
- Heat intolerance, sweating
- Weakness, weight loss, hair loss
- Tachycardia, palpitations
- Hyperdefecation
- Irregular menses
- Goiter / thyroid bruit
- Exopthalmos (Grave's only), lid lag (the lids move more slowly than the eyes)
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Hyperthyroidism (3)
Pre-tibial Myxedema
- Rare manifestation of Graves' disease
- Bilateral, elevated, firm dermal nodules and plaques
- Skin yellow or waxy
- Accumulation of mucopolysaccharides
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Hyperthyroidism (4)
- Risk factors: female, family history, other autoimmune disease
- Lab: Increased T3 and T4, decreased TSH
- Treatment
- Beta blockers
- PTU
- Radioactive iodine
- Surgery
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Thyroid Storm (1)
- A life-threatening complication of hyperthyroidism. May not be directly related to magnitude of excess thyroid hormone
- Precipitating events include
- Withdrawal of antithyroid medications
- Administration of IV contrast
- Thyroid hormone overdose
- Pneumonia
- CVA
- Pulmonary embolus
- Toxemia of pregnancy
- Diabetes
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Thyroid Storm (2)
Thyroid storm is a clinical diagnosis The hallmark is CNS dysfunction
- Other diagnostic criteria include
- Temperature > 38 °C
- Tachycardia out of proportion to the fever
- Exaggerated peripheral manifestations of thyrotoxicosis, including tremor and weakness
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- No laboratory tests distinguish thyroid storm from simple hyperthyroidism – it is a clinical diagnosis
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Thyroid Storm (3)
- Thyrotoxicosis / thyroid storm is associated with
- Elevated free T4 level
- Decreased TSH level
- Hyperglycemia
- Hypercalcemia
- Elevated LFTs
- Low cholesterol
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Thyroid Storm Treatment
- Five step ORDERED approach
- General supportive care: IV fluids, correct electrolyte imbalance, corticosteroids (decrease peripheral conversion of T4 to T3), no ASA (displaces thyroid hormone from thyroglobulin)
- Blockade of peripheral thyroid hormone effects: Propranolol 1 mg to 10 mg titrated to symptoms
- Blockade of thyroid hormone synthesis: PTU (also inhibits peripheral conversion of T4 to T3)
- Blockade of thyroid hormone release: iodine given one hour after PTU
- Identification and treatment of precipitating events
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Apathetic Thyrotoxicosis
- Rare disorder seen in elderly patients
- Lethargy, slowed mentation, apathetic facies
- Goiter is usually present
- Droopy eyelids are common
- No exophthalmos, stare or lid lag
- Symptoms of apathetic hyperthyroidism may be masked because of underlying organ dysfunction
- Resting unexplained tachycardia
- Resistant atrial fibrillation and CHF are common
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Hypothyroidism (1)
- Causes
- Treatment of Graves' disease
- Iodine deficiency in diet
- Autoimmune destruction of thyroid gland (e.g. Hashimoto's)
- Lithium therapy for bipolar disorder
- Amiodarone
- Pituitary and hypothalamic disorders (rare)
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FirstRanker.comHypothyroidism (2)
- Signs and symptoms
- Weakness, lethargy
- Cold intolerance
- Hypothermia
- Weight gain
- Constipation
- Dry, thick skin
- Generalized nonpitting edema (myxedema)
- Prolonged, heavy periods
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Hypothyroidism (3)
- Clinical signs of severe hypothyroidism include
- Dermatologic: coarse, waxy skin, loss of lateral third of eyebrows, scant pubic hair, puffy face and extremities (myxedema)
- CNS: slowed mentation, altered mental status, psychosis ("myxedema madness"), coma
- Cardiac: CHF, bradycardia, hypotension, cardiomegaly, pericardial effusion, low voltage
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Hypothyroidism (4)
- Lab
- Low T4, elevated TSH (unless problem with hypothalamus or pituitary)
- Elevated lipids
- Hyponatremia (dilutional)
- Anemia
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- Myxedema coma
- Hypoxemia
- Hypothermia
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Myxedema Coma (1)
- The end of the spectrum of hypothyroidism
- Life-threatening, rare, elderly females, winter
- Precipitating factors include
- Stressors: MI, infections, trauma, cold exposure
- Drugs are metabolized slower and therefore have increased effects (narcotics, tranquilizers, beta blockers, amiodarone)
- Non-compliance with thyroid replacement
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Myxedema Coma (2)
- Signs
- "Hung up" reflexes (prolonged relaxation phase of DTRs)
- Hypothermia
- Non-pitting periorbital edema (puffy eyelids)
- Generalized non-pitting edema
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Myxedema Coma (3)
- Treatment
- Supportive care: Rewarming, fluid support, search for underlying cause
- Specific treatment
- IV thyroxine (T4). May require large doses
- IV T3 is not recommended (can cause V-tach)
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- Corticosteroids (because of possible unrecognized adrenal or pituitary insufficiency)
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Adrenal Gland
- Clinical manifestations primarily due to
- Cortisol (affects metabolism of most tissues, glucose regulation, increases blood glucose)
- Aldosterone (renal Na+ reabsorption & K+ excretion)
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Adrenal Insufficiency (1)
Primary Adrenal Failure
- Idiopathic (autoimmune): Addison's Disease
- Infiltrative, infectious
- Sarcoid, amyloid
- TB, fungal, septicemia
- Hemorrhage, infarction
- Neoplastic
- Drugs (etomidate)
- Bilateral adrenal failure is associated with meningococcemia (Waterhouse-Friderichsen)
- Presents with abdominal pain, vomiting, fever, hypotension
- Diagnosis by serum cortisol level or corticotropin stimulation test
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Hyperpigmentation is seen in Addison's disease
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Adrenal Insufficiency (2)
- Secondary adrenal failure
- Due to hypopituitarism
- Tertiary adrenal failure
- Usually iatrogenic from prolonged steroid use (most common cause overall)
This download link is referred from the post: MBBS Lecture Notes for all subjects (updated for 2021 syllabus) - All universities
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- Usually iatrogenic from prolonged steroid use (most common cause overall)