Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

AGACNP Board Review > Endocrinology > Flashcards

Endocrinology Flashcards

(56 cards)

Start Studying
1
Q

What is Diabetes Mellitus

A

A metabolic disease resulting from the breakdown in the ability of the body to produce or utiliza insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pathophysiology of Diabeties Mellitus type 1

A
  1. Most commonly seen in adolecent
  2. Associated with the presence of human leukocyte antigens
  3. Islet cell antibodies found in approximately 90% of patients within the first year
  4. Ketone development usually occurs
  5. Believed to be the result of an infectious or toxic insult to pancreatic B cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Signs and symptoms of T1DM

A
  1. Polyuria
  2. Polydipsia
  3. Polyphagia
  4. Nocturnal enuresis
  5. Weight loss
  6. Weakness/Fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Lab/Diagnostivs for T1DM & T2DM

A
  1. Fasting glucose greater than 126
  2. Random plasma glucose greater than 200 with signs of hyperglycemia
  3. Plasma glucose great that 200 after glucose load
  4. Hgb A1C greater than 6.5%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Management of T1DM

A
  1. Obtain baseline of the following
  2. Age of onset
  3. Obesity
  4. Cardiac risk factors
  5. Presence of ketomnes
  6. Diagnostic markers
  7. Lipid panel
  8. ECG
  9. Renel Studies
  10. Baseline Physical Exam
  11. Basal Insulin in addition to Mealtime doses and correction factor insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the somgyi effect?

A

Nocturnal hypoglycemia stimulates a surge of counter regulatory hormones which raise blood pressue

Treatment: Reduce or omit the at bedtime dose of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the Dawn Phenomenon?

A

Happens when the tissues becomes desentized to insulin.Glucose gradually increases overnight resulting in a high AM blood sugar

Treatment: Add or increase the at bedtime dose of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathophysiology of T2DM

A
  1. Most common type of diabeties
  2. Circulating insulin is not enouigh to meet metabolic needs
  3. Main cause is tissue insensitivity or insulin secretory defect
  4. Associated with obesity and metabolic syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Signs and symptoms of T2DM

A
  1. Insidious onset of hyperglycemia
  2. Polyuria
  3. Polydipsia
  4. Reccurent vaginitis
  5. Peripheral neuropathy
  6. Blurred vision
  7. Chronic skin infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Management for T2DM

A
  1. Obtain baseline data
  2. Weight control and exercise
  3. Pharmacotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pharmacotherapy for diabeties

A
  1. Biguanide
  2. GLP-1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What medication are biguanide?

A

Metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What medication are GLP-1 agonists

A
  1. Dulaglutide
  2. Exanatide
  3. Liraglutide
  4. Semaglutide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is DKA?

A

Diabetic ketoacidosis is a state of intracellular dehydrationas result of elevated blood glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Signs and symptoms of DKA

A
  1. Polyuria
  2. Nocturia
  3. Polydipsia
  4. Weakness
  5. Fatigue
  6. Nausea/Vomiting
  7. Kussmauls Breathing
  8. ALOC
  9. Fruity Breath
  10. Orthostatic hypotension with tachycardia
  11. Poor skin turgor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is HHS?

A

Hyperosmolar hyperglycemic state is a condition of marked elevated glucose with severe intracellular dehydration without ketone production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Lab/Diagnostics of DKA

A
  1. Hyperglycemia
  2. Ketonemia
  3. Ketonuria
  4. Glycosuria
  5. Metabilic Acidosis
  6. Elevated Hct
  7. Elevated BUN/Creat
  8. Hyperkalemia
  9. Leukocytosis
  10. Hyperosmoality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Management of DKA

A
  1. Protect the airway
  2. Administer O2
  3. At least 1 L of normal saline within the first hour
  4. Transition to 250-500 mL/h until euvolemic
  5. When gllucose is less than 250, transition to D51/2NS to prevent hypoglycemia
  6. Initiate insulin therapy at 0.1u/kg
  7. Correct acidosis with NACHO3
  8. Hourly urinary output monitoring
  9. Supportive care
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Hyperosmoality conversion

A

2[Na(mEq/L) + K (mEq/L)] + glucose (mg per dL/18) + BUN (mg per dL)/2.8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Signs and symptoms of HHS

A
  1. Polyuria
  2. Weakness
  3. ALOC
  4. Hypotension
  5. Tachycardia
  6. Poor skin turgor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Lab/Diagnositcs of HHS

A
  1. Serum glucose greater than 600
  2. Hyperosmolality
  3. Elevated BUN and Cr
  4. Elevated Hgb A1c
  5. Normal pH
  6. Normal AG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Management of HHS

A
  1. Protect the airway
  2. Administer O2
  3. Same fluid protocol as DKA
  4. Same Insulin protocol as DKA
  5. Supportive care
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is hyperthyroidism

Study These Flashcards
A
  1. Commonly seen in women
  2. Onset between 20-60
  3. Usually presents as Grave Disease
22
Q

What are some causes of hyperthyroidism

Study These Flashcards
A
  1. Toxic adenoma
  2. subacute thyroiditis
  3. TSH secreting tumor
  4. High dose amiordarone
23
Signs and symptoms of hyperthyroidism
1. Nervousness 2. Anxiety 3. Increased sweating 4. Fatigue 5. Emotional Lability 6. Fine tremors 7. Hyperflexion of DTR 8. Increased appetite 9. Smooth, warm, moist velvety skin 10. Fine/thin hair 11. Exophthalmos 12. Lid lag 13. Tachycardia 14. Heat intolerance 15. Atrial Fibrillation
24
Lab/Diagnostics for Hyperthyroidism
1. TSH assay is low 2. Serum T3, T4, free thyroxine is elevated 3. T3 will definitely be elevated 4. Serum ANA is elevated 5. Thyroid radioactive iodine uptake and scan to identifiy cause 6. MRI of the orbits to assess for Grave's Disease
25
Management for hyperthyroidism
1. Specialist referral 2. Propranolol up to 80 mg QID 3. Thiourea drugs like Methimazole 4. Radioactive iodine 131-1 to destroy goiters 5. Thyroid surgery 6. Lugol solution
26
Treatment for thyroid crisis
Propylthiouracil 150-250 every 6 hours Methimazole 15-25 every 6 hours Logol or Sodium iodine + Propranolol + Hydrocortisone
27
Etiology of hypothyroidism
Primary disease of the thyroid gland Pituitary deficiency of TSH Deficiency of TRH Iodine deficiency Hashimotos Thyoiditis Damage to the gland
28
Signs and symptoms of hypothyroidism
1. Weakness 2. Muscle fatigue 3. Arthralgia 4. Cramps 5. Cold intolerance 6. Constipation 7. Weight gain 8. Dry skin 9. Hair loss 10. Brittle nails 11. Puffy eyes 12. Edema of the face and hands 13. Bradycardia 14. Slowed DTRs 15. Hypoactive bowel sounds
29
Lab/Diagnostics for hypothyroidism
1. Elevated TSH 2. Low T4 3. Resin T3 4. Hyponatremia 5. Hypoglycemia
30
Management of hypothyroidism
Levothyroxine
31
Management of Myxdema coma
1. Protect airway 2. Fluid replacement 3. Synthroid 400 mcg IV loading dose and then 100 QD 4. Support hypotension 5. Rewarming blankets 6. Symptomatic care
32
Etiology of Cushing syndrome
It is usually caused by adrenocorticotropic hormone hypersecretiono by the pituitary Adrenal tumors Chronic administration of glucocorticoids
33
Signs and symptoms of Cushing Syndrome
1. Central obesity 2. Moon face with buffalo hump 3. Acne 4. Poor wound healing 5. Purple striae 6. Hirsutism 7. Hypertension 8. Weakness 9. Amenorrhea 10. Impotence 11. Headache 12. Polyuria 13. Thirst 14. Labile mood 15. Frequent Infections
34
Lab/Diagnostics for Cushing Syndrome
Hyperflycemia Hypernatremia Hypokalemia Glycosuria Leukocytosis Elevated plasma cortisol Dexamethasone suppresion Serum ACTH elevation
35
Management of Cushing Syndrome
1. Discontinue medication induing the adrenal crisis 2. Transsphenoidal resection of a pituitary adenoma 3. Surgical removal of adreanal tumors 4. Resection of ACTH secreting tumors 5. Manage electrolyte balance
36
Causes of Addisons disease or Adrenal Crisis
1. Deficient cortisol, adrogens, and aldosterone 2. Autoimmune destruction of the adrenal gland 3. Metastatic cancer 4. Bilateral adrenal hemorrhage 5. Pituitary failure resulting in decreased ACTH
37
Signs/Symptoms of Adrenocortical Insufficiency
1. Hypigmentation in the buccal mucosa and skin creases 2. Diffuse tanning and freckles 3. Orthostasis and hypotension 4. Scant axillary and pubic hair 5. Rapid worsening of chronic signs and symptoms 6. Fever 7. ALOC
38
Lab/Diagnostics for Adrenocortical insufficiency
1. Hypoglycemia 2. Hyponatremia 3. Hyperkalemia 4. Elevated ESR 5. Lymphocytes 6. Plasma cortisol 7. Cosyntropin
39
40
Inpatient management of adrenocortical insufficiency
Hydrocortisone D5NS at 500mL/h Treat underlying cause which is usually infection
41
Etiology of SIADH
1. Release of ADH occurs independently of osomolality or volume dependent stimulation 2. Innapropiate water retention 3. Tumore production of ADH 4. Skull fracture/Head trauma 5. CNS disorder 6. Chronic Lung disease
42
Signs and symptoms of SIDAH
1. Neurologic changes 2. Headache 3. Seizure 4. Coma 5. Decreased DTRs 6. Weight Gain 7. Edema 8. Nausea 9. Vomiting 10. Cold Intolerance
43
Lab/Diagnostics for SIADH
1. Hyponatremia 2. Decreased serum osmolality 3. Increased urine osmoality 4. Urine sodium greater than 20 5. Renal, cardiac, and thyroid function is normal
44
Management for SIADH
1. Treat underlying cause 2. If serum NA is greater than 120, restrict total fluids to 1000 mL/24h and monitor 3. If serum NA is between 110-120 without neuro symptoms, restrict fluids to 500 mL/24h and monitor 4. If serum NA is less than 100 or neuro symtpoms are present, replace with isotonic or 3% normal saline and furosemide. Replace NA and K losses hourly and replace
45
What are the different types of DI
1. Central 2. Nephrogenic 3. Psychogenic
46
Etiology of central diabeties insipidus
1. Damage to hypothalamus or pituitary 2. Surgical damage 3. Accidental trauma 4. Infections 5. Metastatic carcinoma
47
Etiology of nephrogenic diabeties insipidus
1. Genetic X-linked trait 2. Pyelonephritis 3. K+ depletion 4. Sickle cell anemia 5. Chronic hypercalcemia 6. Medications
48
Signs and symptoms of diabeties insipidus
1. Thirst/craving for water 2. Polyuria 3. Nocturia 4. Weight loss 5. Fatigue 6. ALOC 7. Dizziness 8. Elevated temperture 9. Tachycardia 10. Hypotension 11. Poor turgor 12. Dry mucous membranes 13.
49
Lab/Diagnostics for diabeties insipidus
1. Hypernatremia 2. Elevated BUN/Creatinine 3. Elevated serum osmolality 4. Decreased urine osmoalilty 5. Low urine spevific gravity 6. Vasopressin challenge test for central DI 7. Consider MRI for lesion
50
Management of diabeties insipidus
1. If serum sodium is above 150, give D5W IV to replace 1/2 volume deficit in 12-24 hours 2. DDAVP 1-4 mcg IV or SQ QD or Q12 3. Maintenance dose of DDAVP 10 ug every 12-24h intranasally
51
What is a pheochromocytoma?
A pheochromocytoma is a rare, serious disease resulting from excess catecholamine release, characterized by paroxysmal or sustained hypertension. Usually due to a tumor of the adrenal medulla
52
Signs/symptoms of pheochromocytoma
1. Hypertension 2. Diaphoresis 3. Hyperglycemia 4. Severe Headaches 5. Palpitations 6. Diaphoresis 7. Tremor 8. Tachycardia 9. Wegiht loss 10. Postural hypotension
53
Lab/Diagnostics for pheochromocytoma
1. TSH is normal 2. Plasma-free metanephrines 3. 24-hour metanephrine urine 4. CT of adrenal glands
54

AGACNP Board Review (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions