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Medical Emergencies > Endocrine and Metabolic Emergencies > Flashcards

Endocrine and Metabolic Emergencies Flashcards

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USMLE® Step 1 flashcards
1
Q

hyperglycemia

A
  • elevated sugar level
  • an issue
  • can present the same as someone with hypoglycemia
  • can become unconscious
  • hypotensive
  • dehydrated -> give fluids
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2
Q

glucose metabolism

A
  • hyperglycemia
  • hypoglycemia
  • diabetic ketoacidosis (DKA)
  • hyperglycemic hyperosmolar syndrome
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3
Q

hypoglycemia

A
  • low blood sugar
  • the number doesnt really matter -> two people will glucose level is 10 can have very different symptoms
  • normal range 60-120
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4
Q

diabetic ketoacidosis (DKA)

A
  • build up of ketones in the blood
  • commonly seen in kids
  • high blood sugar -> 500
  • hypotensive
  • dehydrated
  • fluid resuscitation
  • occurs in absence or near absence of insulin
  • NIDDM (type 2) at risk during catabolic stress or when insulin dependent
  • common causes include medication non-compliance, infection
  • mortality- 9-14% -> increases with age > 65 -> 24-40%
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5
Q

hyperglycemic hyperosmolar syndrome

A
  • very high blood sugar
  • can be as high as 1000
  • unconscious or unresponsive
  • aggressive management
  • treat with fluids, insulin
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6
Q

insulin

A
  • lowers blood sugar
  • give to hyperglycemic patients
  • always monitor when giving in case pt becomes severely hypoglycemic
  • dominant hormone when blood glucose level is high
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7
Q

glucose / dextrose / glucagon

A

give to patients with hypoglycemia

  • dextrose is given IV
  • dominant hormone when blood glucose level is low
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8
Q

pancreas*

A
  • metabolism of cells
  • alpha cells
  • beta cells
  • delta cells
  • gamma cells
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9
Q

alpha cells

A
  • stimulate release of glucagon and glycogen stores

- promote gluconeogenesis

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10
Q

beta cells

A

-stores and release insulin

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11
Q

delta cells

A

-inhibit glucagon and insulin via somatostatin

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12
Q

gamma cells

A

-secrete pancreatic polypeptide

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13
Q

pancreas and autonomic system

A

Activity of the cells in the islets is affected by the autonomic nervous system:
Sympathetic(adrenergic)α2: decreases secretion frombeta cells, increases secretion fromalpha cells, β2: increases secretion frombeta cellsParasympathetic(muscarinic)M3: increases stimulation ofalpha cellsandbeta cells[14]
Voltage-gated calcium channelsandATP-sensitive potassium ion channelsare embedded in the cell surface membrane of beta cells. These ATP-sensitive potassium ion channels are normally open and the calcium ion channels are normally closed. Potassium ions diffuse out of the cell, down their concentration gradient, making the inside of the cell more negative with respect to the outside (as potassium ions carry a positive charge). At rest, this creates apotential differenceacross the cell surface membrane of -70mV

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14
Q

type 1 diabetes mellitus

A
  • also called juvenile or insulin-dependent diabetes mellitus (IDDM)
  • hyperglycemia
  • characterized by low production of insulin
  • closely related to heredity
  • results in pronounced hyperglycemia
  • symptoms of untreated type 1 DM include polydipsia (drinking a lot), polyuria (urinating a lot), polyphagia (eating a lot), weight loss, and weakness (TRIAD*)
  • high ketones in urine
  • untreated or noncompliant patients may progress to ketosis and diabetic ketoacidosis
  • altered mental status and dehydration may progress if left untreated
  • do they have dry mouth, skin turgor, blood flow,
  • give 500-100CC of fluid for adults
  • 20CC per kilo for children (weight based)
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15
Q

type 2 diabetes mellitus

A
  • not insulin dependent
  • also called adult-onset or non-insulin-dependent diabetes mellitus (NIDDM)
  • results from decreased binding of insulin to cells
  • related to heredity and obesity
  • most common form of diabetes
  • accounts for 90% of all diagnosed diabetes patients
  • less risk of fat-based metabolism
  • results in less-pronounced hyperglycemia
  • hyperglycemic hyperosmolar nonketonic acidosis
  • managed with dietary changes and oral drugs to stimulate insulin production and increased receptor effectiveness
  • give them oral medications like metformin
  • dependent on environment -> diet
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16
Q

type 1 vs type 2

A
  • type 1:
  • sudden
  • any age (mostly young)
  • thin of normal body
  • ketoacidosis is common
  • autoantibodies are present
  • endogenous insulin is low or absent
  • less prevalent
  • type 2:
  • gradual onset
  • mostly in adults
  • often obese
  • ketoacidosis is rare
  • autoantibodies are absent
  • endogenous insulin is normal, decreased or increased
  • more prevalent -> 90%-95%
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17
Q

diabetic ketoacidosis (DKA) presentation

A
  • anorexia
  • nausea
  • emesis
  • polyuria
  • kussmaul respirations- deep, fast labored breathing
  • fruity breath
  • deterioration mental status
  • hypotension
  • progressive acidosis
  • chest and/or abdominal pain
  • children can decompensate very fast!
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18
Q

DKA- associated abnormalities

A
  • electrolyte imbalances
  • affects the heart and arrhythmias -> can cause death
  • sodium
  • chloride
  • potassium
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19
Q

sodium abnormalities - DKA

A
  • variable
  • fall by 1.6 for every 100 increasing glucose (pseudohyponatremia)
  • falsely low with hypertriglyceridemia
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20
Q

chloride abnormalities - DKA

A
  • hyper in ketoacidosis
  • can be elevated due to choice of resuscitation fluid
  • hypo associated with severe emesis
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21
Q

potassium abnormalities - DKA

A
  • total body hypokalemia
  • intravascular K+ high with acidosis
  • at high risk for severe hypokalemia
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22
Q

DKA management: fluid resuscitation

A
  • generally severely dehydrated
  • lactated ringers preferred over NS
  • add dextrose once BS < 300
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23
Q

DKA management insulin

A
  • .15 u/kg of regular insulin IV gtt
  • continue until beta-hydroxybutyrate in blood less then 1 or resolved AG
  • transition to sub-Q insulin with overlap of 1-2 hours
24
Q

DKA management - potassium

A
  • aggressive KCl replenishment and maintenace

- do not start insulin until K > 3.5-5

25
Q

DKA management: sodium bicarbonate

A
  • never give sodium bicarbonate
  • NaHCO3 + H+ -> H2CO3 -> CO2 + H2O
  • worsens intracellular acidosis as already man respiratory compensation
  • treat underlying cause
26
Q

DKA complications

A
  • Hypotension and shock
  • Thrombosis
  • Cerebral edema (In Pediatrics… maybe)
  • Renal failure
  • Hypoglycemia
27
Q

hyperglycemic hyperosmolar syndrome

A
  • Present with severe dehydration without ketosis and acidosis
  • Glucose > 1000
  • Coma, seizures, tremors, hemiplegia
  • Causes:
  • infection
  • MI
  • hemorrhage and trauma
  • burns
  • Similar to DKA treatment, but even more fluid depleted
28
Q

hypoglycemia

A
  • True medical emergency resulting from low blood glucose levels; rarely seen outside diabetics.
  • By the time signs and symptoms develop, most of the body’s stores have been used.
  • Diabetics with kidney failure are predisposed to hypoglycemia.
  • pale
  • shaky, hast heartbeat, sweating, dizzy, anxious, hungry, irritable, blurry vision, weakness or fatigue, headache
29
Q

diabetic ketoacidosis vs hyperglycemic hyperosmolar syndrome

A
  • diabetic ketoacidosis:
  • profound ketoacidosis
  • 250-600 mg/dL
  • young*
  • acute
  • severe dehydration
  • insulin is low
  • hyperglycemic hyperosmolar syndrome:
  • minimal or none ketoacidosis
  • > 900 mg/dL
  • elderly*
  • chronic
  • profound dehydration
  • insulin may be normal
30
Q

hypoglycemia treatment

A
  • glucose
  • glucagon
  • dextrose (IV)
31
Q

look at charts in power point*

A
32
Q

thyroid dysfunction

A
  • hypothyroidism
  • thyrotoxicosis
  • thyrotoxicosis crisis
  • thyroid storm
  • affects the metabolism
33
Q

hypothyroidism

A
  • low BP
  • bradycardia
  • fatigued
  • iodine deficiency
  • thyroidectomy can cause
  • hair loss
  • dry skin
  • intolerance to cold
  • weight gain
34
Q

hyperthyroidism

A
  • hypertensive
  • tachycardia
  • everything is elevated
  • weight loss
35
Q

hypothyroidism therapy

A
  • uncomplicated
  • outpatient treatment
  • synthroid
  • age dependent
  • young- 50-100 ug/d
  • old 12.5-25 ug/d
  • check TSH at 4-6 weeks
  • change doses 12.5 to 25 ug increments
  • get blood checked by endocrinologist often
  • look for underlying infections
  • correct hypothermia
  • blood volume restoration
  • monitor electrolytes
  • glucose replacedment
  • check for drug toxicity (digoxin etc)
36
Q

throxine replacement

A
  • loading dose 300-500 uq IV
  • no CV complications in critically ill
  • ? higher mortality in high T3 toxicosis
  • maintenance 50-100ug/d
37
Q

causes of hyperthyroidism

A
  • graves disease
  • toxic multinodular goiter (toxic nodular struma)
  • independent or solitary toxic adenoma
  • thyroiditis or inflammation of the thyroid gland
38
Q

hyperthryoidism symptoms

A
  • fine, straight hair
  • bulging eyes
  • facial flushing
  • tachycarida
  • high systolic pressure
  • weight loss
  • increased diarrhea
  • menstrual changes
  • localized edema
39
Q

thyrotoxicosis

A
  • high mortality rate
  • thyroid crisis “storm”
  • life threatening 10-20% mortality
  • precipitation factors:m
  • infection
  • thyroid manipulation (operation, palpation)
  • metabolic disorders (DKA)
  • trauma
  • MI
  • PE
  • pregnancy
39
Q

thyrotoxicosis

A
  • high mortality rate
  • thyroid crisis “storm”
  • life threatening 10-20% mortality
  • everything is elevated
  • precipitation factors:
  • infection
  • thyroid manipulation (operation, palpation)
  • metabolic disorders (DKA)
  • trauma
  • MI
  • PE
  • pregnancy
40
Q

management of thyroid storm

A
  • pharmacologic control:
  • Inhibit conversion of T4 to T3
  • consider steroids or PTU
  • ipodate sodium (Oragrafin) highly effective
  • caution long-term use (“escape”
  • Reduction of hyperadrenergic state
  • propranolol (historical)
  • cautious of B-blockers in CHF
  • Removal of T4
  • plasmaphresis or hemoperfusion
  • emergent thyroidectomy
41
Q

complications of hyperthyroidism

A
  • atrial arrhythmias
  • most convert within 3 weeks of euthyroidism
  • never after 4 months
  • no prospective study on anticoagulation
  • CVA age dependent not atrial fib dependent
  • clots can form!
  • CHF
  • malnutrition/dehydration
  • metabolic failure
  • drug metabolism
42
Q

acid-base disorders

A
  • Body can adjust for pH fluctuations
  • Buffering systems used for short-term pH control
  • “Ties up” H+
  • Respiratory and renal systems used for long-term acid-base balance
  • Removes Hydrogen from body
  • Manipulate pH with CO2, HCO3, and H secretion/retention
  • Combination of buffer, respiratory, and renal systems maintain pH within normal 7.35–7.45 range
43
Q

buffer systems

A

-respiratory
-renal
-maintain metbaolism
-

44
Q

acid-base disorders***

A
  • normal values
  • pH- 7.35-7.45
  • PCO2- 35-45 mmHg
  • HCO3- 22-26 mEg/L
45
Q

alkalotic*

A
  • higher pH than 7.45
  • above 8 is death
  • higher than 45 CO2
46
Q

acidotic*

A

pH is less then 7.35

-lower than 35 PCO2

47
Q

respiratory acidosis

A
  • pH is less then 7.35
  • PaCO2 is higher than 45
  • HCO3 is normal (22-26)
  • shallow breathing
  • CO2 is being retained
  • not breathing fast
  • treat with supplemental oxygen
48
Q

respiratory alkalosis

A
  • pH is greater than 7.45
  • PaCO2 is less then 35
  • HCO3 is normal (22-26)
  • hyperventilating
  • anxiety attack
  • give paper bag, or put on the o2 mask but not actually turn it on
49
Q

metabolic acidosis

A
  • pH is less than 7.35
  • PaCO2 is normal (35-45)
  • HCO2 is less then 22
50
Q

metabolic alkalosis

A
  • pH is higher than 7.45
  • PaCO2 is normal (35-45)
  • HCO3 is higher than 26
51
Q

metabolic acidosis /alkalosis

A
  • look at the underlying cause!
  • do they have sepsis
  • pneumonia
  • what is causing this
  • pt wont present in a certain way you must treat the underlying cause
52
Q

buffer mechanisms

A
  • dissolved compounds that stabilize the pH of a solution by adding or removing H+
  • four types of buffering systems in human body:
  • protein buffering
  • hemoglobin buffering
  • carbonic acid-bicarbonate buffering phosphate buffering -> phosphate the most common intracellular buffer
53
Q

rhabdomyolysis

A
  • a breakdown of muscle tissue that causes myoglobin to be released into the bloodstream, causing kidney damage and renal failure
  • S/S dark colored urine, weakness, and muscle pain
  • urine is dark bc kidney is filtering
  • causes:
  • prolonged periods of immobilization
  • trauma
  • crush injuries
  • drug abuse
  • electrolyte abnormalities
54
Q

diagnosis of rhabdomyolysis

A
  • myoglobin/protein in the urine
  • elevated creatine levels
  • comprehensive history including a physical exam
55
Q

rhabdomyolysis treatment

A
  • fluid hydration
  • osmotic diuretics
  • bicarbonate infusion
56
Q

conclusion

A
  • Important Metabolic Disorders- Hypothyroidism vs. Hyperthyroidism
  • What to expect in patient presentation and vitals
  • Types of hyperthyroidism
  • Thyrotoxicosis vs Thyroid Storm
  • Rhabdomyolysis:
  • Signs and symptoms as it relates to this condition
  • Various causes of this condition
  • Diabetes Mellitus:
  • Difference between Type 1 and Type 2 DM
  • Pathophysiology and treatment of Hypoglycemia
  • DKA and HHNK:
  • Three P’s as it relates to assessment
  • Treatment Plan for both conditions
  • Pancreas:
  • Alpha, Beta, and Delta Cells
  • Acid-Base Disorders:
  • Know the values as it relates to the buffer system
  • Acidosis: Metabolic and Respiratory
  • Alkalosis: Metabolic and Respiratory
  • What are the four major buffer mechanisms?
  • When can death occur as a result of the buffer system?

Medical Emergencies (16 decks)

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