Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Board Exam > Endocrine > Flashcards

Endocrine Flashcards

1
Q

When a patient presents with unexplained weight loss, what should always be on your differential?

A

Endocrine cause
- uncontrolled DM 1
- adrenal insufficiency
- pheochromocytoma
- hyperthyroidism
Malignancy (esp in elderly)

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

Diabetes Mellitus

A

a syndrome of disordered metabolism and inappropriate hyperglycemia due either to a deficiency of insulin secretion, or to a combination of insulin resistance and inadequate insulin secretion to compensate

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

Type 1 DM: causes

A

Causes: pancreatic islet B cell destruction predominantly by an autoimmune process
-90% are related to autoimmune attack on islet cells associated with certain HLA genes
-the other 10% are idiopathic - no islet cell destruction

islet autoantibodies are often present

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

Type 2 DM: causes

A

Caused by either tissue insensitivity to insulin or an insulin secretory defect resulting in resistance and/or impaired insulin production

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

Type 1 DM: treatment

A

eucaloric diet
preprandial rapid acting insulin plus basal intermediate or long acting insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Type 2 non-obese DM: treatment

A

eucaloric diet alone
OR
diet plus oral agents

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

Type 2 obese DM: treatment

A

weight reduction
hypocaloric diet plus oral agents and insulin

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

metformin: mechanism

A

acts on the liver to reduce gluconeogenesis and causes a decrease in insulin resistance
- lowers basal and postprandial glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

metformin: advantages

A

Not associated with weight gain
Low risk of hypoglycemia
Reduces LDL, triglycerides
No effect on BP
Inexpensive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

metformin: disadvantages

A

-increased risk of GI side effects
-risk of lactic acidosis increased for people with stable or acute heart failure, liver disease, alcoholism, or recovering from major surgery
-increased risk of vitamin B12 deficiency
-less convenient dosing

Discontinue 1-2 days before receiving iodinated radio contrast medium; may cause lactic acidosis (BLACK BOX WARNING)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Dipeptidyl peptidase-4 (DPP-4) inhibitors (sitagliptin, saxagliptin): mechanism

A

Inhibits DPP-4 from degrading GLP-1, increasing its blood concentration which causes increased insulin to be released from beta cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Dipeptidyl peptidase-4 (DPP-4) inhibitors (sitagliptin, saxagliptin): advantages

A

weight neutral
fewer GI side effects
rarely causes hypoglycemia

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

Dipeptidyl peptidase-4 (DPP-4) inhibitors (sitagliptin, saxagliptin): disadvantages

A

expensive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Glycosurics (canagliflozin) (SGLT-2 inhibitors): mechanism

A

block the re-uptake of glucose in the renal tubules, promoting loss of glucose in the urine

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

Glycosurics (canagliflozin) (SGLT-2 inhibitors): advantages

A

mild weight loss
mild reduction in blood sugar levels
minimal risk of hypoglycemia

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

Glycosurics (canagliflozin) (SGLT-2 inhibitors): disadvantages

A

vaginal candidiasis
UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

GLP agonists (Liraglutide): mechanism

A

bind to a membrane GLP receptor, causing increased insulin to be released from beta cells
Reduce glucagon
Slow gastric emptying

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

GLP agonists (Liraglutide): advantages

A

significant weight loss
low risk for hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

GLP agonists (Liraglutide): disadvantages

A

-increased risk of pancreatitis
increased risk for thyroid cancer (BLACK BOX WARNING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

DKA: mechanism

A

Lack of insulin + elevated glucagon –> increased levels of glucose by the liver
Glucose spills over into the urine, taking water and solutes (Na+ and K+) along with it
This leads to polyuria, dehydration, polydipsia
Absence of insulin –> release of FFAs from adipose tissue, which are converted into ketone bodies and cause metabolic acidosis
Initially, the body buffers the change with the bicarbonate buffering system, but this is quickly overwhelmed and other mechanisms must work to compensate for the acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

DKA: labs/Dx

A

Essentials of diagnosis:
-Hyperglycemia >250mg/dL
-Acidosis with venous pH <7.3 (arterial pH <7.25)
-Serum bicarbonate (15mEq/L) low
-Serum positive for ketones (beta-hydroxybutane >1.5)

Hyperkalemia
BUN/Cr elevated
Anion gap >15

Hct elevated
Leukocytosis

Low pCO2
Elevated serum osmolality (>330 mosm/L)

Ketonemia, ketonuria
Glycosuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

DKA: Treatment

A

Unable to protect airway or comatose: intubate immediately

  1. Restore fluid deficit: 20-40cc/kg boluses
    - 1 L NS in the first hour, then 500 ml/hr
    - If glucose >500, use 1/2 NS after first hour
    - When glucose <250mg/dL, D5 1/2NS to prevent hypoglycemia
  2. Treat hypokalemia before giving insulin
  3. Treat hyperglycemia: Regular insulin
    - 0.1 units/kg IV bolus
    - 0.1 units/kg/hr IV gtt
    • insulin gtt titrated hourly according to delta glucose
      - If glucose does not fall by at least 10% after the first hour, repeat bolus
  4. Acidosis
    - if pH <7.1, start bicarb drip 44-48 mEq in 900 ml 1/2 NS until pH >7.1
    -overcorrection can lead to hypokalemia d/t transcellular shift of K+ when the pH changes too fast

Identify and treat underlying infection

ICU

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

HHNK

A

Hyperglycemic/hyperosmolar non-ketotic state
State of greatly elevated serum glucose, hypoerosmolality, and severe intracellular dehydration without ketone production
Patients cannot produce enough insulin to prevent severe hyperglycemia, osmotic diuresis and extracellular fluid depletion

Similar to DKA (develops d/t insulin deficiency) but usually occurs over days to weeks
More common in type 2 diabetes rather than type 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

HHNK is often precipitated by

A

non-compliance
infection
MI
stroke
surgery
steroid administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

HHNK: essentials of diagnosis

A

Hyperglycemia >600mg/dL
elevated BUN/Cr
serum bicarb >15mEq/L
elevated Hb A1c
serum osmolality >310mosm/L

no acidosis, pH >7.3
normal anion gap, <14
no ketosis, b-hydroxybutyrate <0.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

HHNK: treatment

A

Protect the airway

Dehydration:
- Isotonic IV fluids (6-10L NS) within the first 24 hours
- 1 L in the first hour, then 500 ml/hr
- if glucose >500 mg/dl, use 1/2 NS after the first hour
- when glucose <250 mg/dl, change to D5 1/2 NS to prevent hypoglycemia

Insulin
- Less insulin is usually required- glucose usually decreases with fluids alone so a relatively normal insulin regimen can be given
- 0.1 u/kg regular insulin IV bolus
- 0.1 u/kg/hr gtt
- if glucose does not fall by at least 10% after the first hour, repeat bolus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Hypoglycemia treatment: overdose of metformin

A

octreotide 75mcg SC/IM
Feed the patient
Observe for 12-24 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Hypoglycemia treatment: if there has not been any obvious error made and hypoglycemia persists

A

Consider:
-insulinoma: will require endocrine consult
-beta blocker overdose
-factitious disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Type 1 DM is strongly associated with which antigens?

A

human leukocyte antigens (HLA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Type 1 DM: presentation

A

-polyuria
-polydipsia
-polyphagia
-weight loss
-nocturnal enuresis
-weakness, fatigue
-serum glucose >200mg/dL
-ketonemia, ketonuria, or both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Type 2 DM: presentation

A

-age >40
-insidious onset of hyperglycemia
-polyuria
-polydipsia
-women: recurrent vaginitis
-late: peripheral neuropathies, blurred vision
-chronic skin infections, including pruritis
-often associated with HTN, HLD, atherosclerotic disease
-high levels of insulin to prevent ketosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Type 1 and Type 2 DM: labs/Diagnosis

A

At least one:
-Serum fasting (>8 hrs) BG >126 mg/dl on more than one occasion
-Random plasma glucose >200 mg/dl with signs of hyperglycemia (e.g. polyuria, polydipsia, weight loss)
-plasma glucose >200 mg/dl measured 2 hours after a glucose load of 1.75 g/kg (max dose 75g) in an oral glucose tolerance test
-glycated hemoglobin (A1C) >6.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Somogyi Effect and treatment

A

Seen in Type 1 DM

Nocturnal hypoglycemia develops after stimulating a surge of counter regulatory hormones with raise blood sugar
-hypoglycemic at 3am but rebounds with an elevated blood glucose at 7am

Treatment: reduce or omit the bedtime dose of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Dawn Phenomenon and treatment

A

Seen in Type 1 DM

Results when tissue becomes desensitized to insulin nocturnally
-blood glucose becomes progressively elevated throughout the night, resulting in elevated glucose levels at 7am

Treatment: add or increase the bedtime dose of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Risk factors for Type 2 DM

A

waist circumference >40 in in men and >35 in in women
BP >130/85
Triglycerides >150
FBG >100
HDL <40 in men and <50 in women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

DKA: S/Sx

A

CNS depression or coma
Kussmaul’s breathing
Hyptension
Tachycardia
Parched mucous membranes
Abdominal pain, NV
polyuria, including nocturia
polydipsia
weakness/fatigue
fruity breath
orthostatic hypotension with tachycardia
poor skin turgor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

HHNK: S/Sx

A

polyuria
weakness
changes in LOC
hypotension
tachycardia
poor skin turgor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What condition is associated with recurrent nephrolithiasis?

A

hyperparathyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

pheochromocytoma

A

Adrenal mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

pheochromocytoma: risk factors

A

females > males
foods high in tryamine (alcohol, certain cheeses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Pheochromocytoma: S/Sx

A

headache
diaphoresis
hypertension
orthostatic hypotension
tachycardia

leukocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Thyroid tests for screening

A

TSH: most sensitive test for primary hypothyroidism and hyperthyroidism
Free thyroxine (FT4): quite sensitive for hypothyroidism, as T4 is the product of the thyroid itself

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Thyroid testing for nodules

A

Fine-needle aspiration: best diagnostic method for thyroid cancer

123I uptake and scan: “Cold” spots usually indicate a more malignant hypofunctioning nodule

99mTc scan: vascular (more worrisome) vs avascular (less worrisome) nodules

Ultrasound:
-assist in FNA
-cystic lesions are of low-suspicion for cancer
-solid lesions are of high suspicion for cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What to do if you find thyroid nodules

A

Check TSH and T4
More suspicious nodules should be referred for FNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Less worrisome thyroid nodules

A

High TSH, low FT4
older women
cystic appearance on ultrasound
family history of goiter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How does 131I work

A

It is taken up by the remaining thyroid tissue after thyroidectomy and the isotope destroys it
It renders the patient radioactive for a period of time and the patient must quarantine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Hypothyroidism: symptoms

A

fatigue
cold intolerance
constipation
weight gain
depression
menstrual problems
hoarseness
“puffy” appearance to the face, pale complexion, under-eye edema and hyperpigmentation, tongue enlargement, eyebrow thinning
extreme weakness
arthalgias
cramps
dry skin
hair loss
brittle nails
bradycardia
slowed DTRs
hypoactive bowel sounds

48
Q

Hypothyroidism: labs

A

TSH: high in primary, low in secondary
T4: low
resin T3 uptake: decreased
hyponatremia
hypoglycemia

T3 is not a reliable test

49
Q

myxedema

A

late hypothyroidism, can result in myxedema coma

50
Q

myxedema coma

A

Occurs when an already hypothyroid patient is placed under physiologic stress (e.g. infection)
Often results and coexists with acute adrenal insufficiency

51
Q

myxedema coma: Symptoms

A

decreased LOC
hypothermia
hyponatremia
hypoglycemia
hypotension
hypoxia/hypercapnia
bradycardia

52
Q

myxedema coma: labs

A

TSH: very high
FT4: very low
random cortisol: low (reflects adrenal insufficiency)

53
Q

myxedema coma: treatment

A

Protect airway
Fluid replacement as needed

levothyroxine 400mcg IV once, then 100mcg IV daily

If adrenal insufficiency is present: hydrocortisone 100mg IV, then 25-50mg IV q8h

support hypotension
slow rewarming with blankets, avoid circulatory collapse
symptomatic care

54
Q

hyperthyroidism: symptoms

A

tachycardia
tremor
sweating
weight loss, increased appetite
anxiety
loose stools
heat intolerance
irritability
fatigue
menstrual problems
exophthalmos, lid lag
hyperreflexia
smooth, warm, moist velvety skin
fine/thin hair
increased incidence of AFib

55
Q

hyperthyroidism: labs

A

TSH: very low
FT4: high
T3: high
thyroid resin uptake: high
ANA: positive (no evidence of SLE or other collagen diseases)

56
Q

hyperthyroidism: treatment

A

propranolol: symptomatic relief

Thiourea drugs for patients with mild cases, small goiters, or fear of isotopes
-methimazole (Tapazole) 30-60mg/day until FT4 levels return to normal
- propylthiouracil 300-600mg daily in 4 divided doses

131I to destroy the thyroid, then thyroid hormone replacement therapy for life

Thyroid surgery (must be euthyroid pre-op)

Lugol’s solution 2-3 got PO daily x10 days to reduce vascularity of the gland

57
Q

thyroid storm

A

results from untreated hyperthyroidism
can be mistaken for acute mania or psychosis

58
Q

thyroid storm: presentation

A

Fever
Marked tachycardia
Mental status changes
GI disturbances
Profuse diaphoresis
Hyperglycemia

59
Q

thyroid storm: treatment

A

arrhythmias (AF/RVR is the most common): digoxin

propylthyiouracil 150-250mg Q6h OR
methimazole (Tapazole) 15-25mg every 6 hours WITH the following in 1 hour:
-Lugol’s solution 10 gets TID
OR
-sodium iodide 1 g slow IV with:
-propanolol 0.5-2g IV Q4h or 20-120 mg PO q6h with
-hydrocortisone 50mg Q6h with rapid reduction as situation improves

behavioral: benzos

destroy thyroid: 131I or thyroidectomy

60
Q

Subclinical hypothyroidism: labs

A

TSH elevated

61
Q

Subclinical hyperthyroidism: labs

A

TSH low
unbound T4 normal

62
Q

Graves disease: labs

A

TSH low
T3 elevated
T4 elevated

63
Q

Graves disease: presentation

A

Age of onset typically 20-40
More prevalent in females

Goiter
Ophthalmopathy
Fatigue
Heat intolerance
Anxiety
Palpitations
Neck swelling
Eyelid retraction
Exophthalmos
Periorbital edema

Thyroid gland firm and enlarged

64
Q

hyperthyroidism: cause/incidence

A

More common in women (8:1 ratio)
Onset most commonly between 20-40 years old
Graves’ disease is the most common presentation

Other causes:
-toxic adenoma
-subacute thyroiditis
-TSH secreting tumor of the pituitary
-high dose amiodarone

65
Q

hypothyroidism: cause/etiology

A

Most common cause: Hashimoto’s thyroiditis

Primary disease of the thyroid gland
Pituitary deficiency of TSH
Hypothalamic deficiency of thyrotropin-releasing hormone (TRH)
Iodine deficiency
Idiopathic causes
Damage to the thyroid

66
Q

hypothyroidism: management

A

Levothyroxine 50-100 mcg daily, increasing dosage by 25 mcg every 1-2 weeks until symptoms stabilize
- decrease dosage >60 years of age
- initial hair loss may occur

67
Q

parathyroids

A

4 tiny glands within the thyroid that:
-sense levels of calcium in the blood
-secrete parathyroid hormone

68
Q

4 jobs of parathyroid hormone

A

-increasing osteoclastic activity in the bones, which increases delivery of calcium and phosphorous to the bloodstream
-increasing renal tubular reabsorption of calcium
-inhibiting the net absorption of phosphorous and bicarbonate in the renal tubule
-stimulates the synthesis of 1,25-dihydroxycholecalciferol (the active metabolite of vitamin D) in the kidney

These all have the net effect of a rise in the serum ionized calcium

69
Q

Most common cause of hypoparathyroidism

A

accidental injury or removal of the parathyroids during thyroidectomy

70
Q

hypoparathyroidism: symptoms

A

tetany
parasthesias
carpopedal spasms
abdominal cramping

71
Q

hypoparathyroidism: labs

A

serum Ca: low
ionized Ca: low
urine Ca: low
serum Mg: low
PO4(3-): high
alk phos: normal

72
Q

hypoparathyroidism: treatment

A

calcium salts
vitamin D

73
Q

acute hypoparathyroid tetany: treatment

A

intubation/mechanical ventilation if needed
calcium gluconate IV slowly until tetany ceases, then gtt to maintain serum Ca between 8-9 mg/dL
Calcitrol IV daily
transplant cryopreserved parathyroid tissue that was removed during surgery if it was preserved by the surgeon

74
Q

hyperparathyroidism: cause

A

caused by hypersecretion of parathyroid hormone, most often by a parathyroid adenoma

75
Q

hyperparathyroidism: symptoms

A

often asymptomatic but patients often have frequent kidney stones

76
Q

hyperparathyroidism: labs

A

serum Ca: high
urine Ca: high
urine phos: high
serum phos: low to normal
alk phos: normal to high

77
Q

hyperparathyroidism: treatment for acute hypercalcemia

A

fluids
bisphosphonate

78
Q

hyperparathyroidism: treatment for mildly symptomatic disease

A

surgical excision of the affected parathyroid if it can be identified
bisphosphonates to counteract the elevated PTH’s effect on osteoclasts
calcimimetics (Cinacalcet) “fools” the parathyroid into thinking the calcium is very high, thereby lowering the PTH secretion

79
Q

Addison’s Disease: causes

A

caused by destruction or dysfunction of the adrenal glands, resulting in a deficiency of:
- cortisol
- aldosterone
- adrenal androgens (e.g. dehydroepiandrosterone)

Usually caused by
-autoimmune attack of adrenal cortices
-metastatic cancer
-bilateral adrenal hemorrhage (e.g. with anticoagulants)
-pituitary failure resulting in decreased ACTH

80
Q

cortisol

A

increases blood glucose by gluconeogenesis, to suppress the immune system, and to aid in the metabolism of fat, protein, and carbs

81
Q

aldosterone

A

essential for sodium conservation in the kidney, salivary glands, sweat glands, and colon
plays a central role in the homeostatic regulation of BP, Na+, and K+ levels

82
Q

Addison’s disease: Symptoms

A

weakness
easy fatiguability
anorexia
weight loss
N/V/D
amenorrhea
Hyperpigmentation in buccal mucosa and skin creases
Diffuse tanning/bronxzing and freckles
Orthostasis and hypotension
Scant axillary and pubic hair

acute:
-Rapid worsening of chronic signs and symptoms
-fever
-altered LOC

83
Q

Addison’s disease: labs/Dx

A

hypoglycemia
hyponatremia
hyperkalemia
neutropenia
AM serum cortisol levels: low or fail to rise after being given corticotropin (exogenous ACTH)
elevated ESR
lymphocytosis

Cosyntropin stimulation test to r/o Addison’s

84
Q

When should you consider acute Addisonian crisis?

A

Known Addison’s disease or patients on chronic steroids who present with
- hypotension
- hypothermia
- hypoglycemia
- hyperkalemia

85
Q

Cushing’s disease: cause

A

excessive cortisol that is a result of:
- excessive ACTH secretion by the pituitary in the case of a pituitary adenoma
- chronic glucocorticoid use
- adrenal hyperfunction
- adrenal tumors

86
Q

Cushing’s disease: S/Sx

A

moon face
buffalo hump
central obesity
hypertension
muscle wasting
thin skin
purple abdominal striae
acne
poor wound healing
hirsutism
weakness
amenorrhea
impotence
headache
polyuria and thirst
labile mood
frequent infections

87
Q

Cushing’s disease: labs/Dx

A

hyperglycemia
hypernatremia
hypokalemia
glycosuria
leukocytosis

elevated serum cortisol in AM
dexamethasone suppression test to differentiate cause
serum ACTH

88
Q

Cushing’s disease: management

A

If caused by chronic glucocorticoid therapy
- attempt to slowly wean from them if possible

If not caused by glucocorticoids, measure ACTH
- low = adrenal tumor
- CT scan to locate tumor. If it cannot be found, the adrenals should be resected and patient should be placed on hydrocortisone for life
- high = pituitary adenoma
- brain MRI; excise adenoma

89
Q

pheochromocytoma

A

rare condition where a tumor forms (usually in the adrenal glands) that secretes catecholamines (norepinephrine and epinephrine) inappropriately

90
Q

pheochromocytoma: presentation

A

“attacks” of headache, perspiration, palpitations, nausea, chest pain, tremor
often hypertensive and tachycardic
- hypertensive crisis
- ventricular arrhythmias may occur

91
Q

pheochromocytoma: labs and imaging

A

TSH: normal
FT4: normal

24 hour urine: metanephrines, catecholamines, vanillylmandelic acid

CT of adrenals to confirm and localize tumor
PET scan

92
Q

pheochromocytoma: management

A

Surgical removal

Alpha adrenergic medications pre-op
-Phentolamine (Regitine) 1-2mg IV Q5 min until controlled, then 1-5 mg IV every 12-24 hrs
-Convert to PO asap: phenoxybenzamine (Dibenzyline)

Post-op watch for:
-hypotension (d/t depleted catecholamines)
-adrenal insufficiency
-hemorrhage

93
Q

Addison’s disease: outpatient management

A

specialist referral
glucocorticoid and mineralocorticoid replacement
-hydrocortisone
-fludrocortisone acetate (Florinef)

94
Q

Addison’s disease: inpatient management

A

Hydrocortisone 100-300mg IV initially with NS
Replace volume with D5NS at 500 ml/hr x4 hrs

Vasopressors usually ineffective

Treat underlying cause, often infection

95
Q

SIADH: causes/etiology

A

Release of ADH occurs independent of osmolality or volume dependent stimulation
Inappropriate water retention
Tumor production of ADH
CNS disorder: stroke, trauma, infection, psychosis
Chronic lung issue

96
Q

SIADH: S/Sx

A

Neuro changes d/t hyponatremia: mild HA, seizures, coma
Decreased DTRs
Hypothermia
Weight gain/edema
N/V
Cold intolerance

97
Q

SIADH: labs/Dx

A

Hyponatremia
Decreased serum osmolality (<280 mOsm/kg)
Increased urine osmolality (>100 mOsm/kg)
Urine sodium >40 mEq/L

98
Q

SIADH: management

A

Treat underlying cause

Na+ >120 mEq/L: 1000 ml/day fluid restriction and monitor
Na+ 110-120 mEq/L without neuro symptoms: 500ml/day fluid restriction and monitor
Na+ <110 mEq/L or neuro symptoms present, isotonic or hypertonic saline and furosemide at 1-2 mEq/h
-Monitor K and Na losses hourly and replace

99
Q

Diabetes Insipidus: causes/etiology

A

excessive urination and extreme thirst from an inadequate output of the pituitary hormone ADH or the lack of normal response by the kidney to ADH

100
Q

Central DI: causes/etiology

A

Related to pituitary or hypothalamus damage resulting in ADH deficiency
-idiopathic causes
-damage to hypothalamus or pituitary
-surgical damage
-accidental trauma
-infections
-metastatic carcinoma

101
Q

Nephrogenic DI: causes/etiology

A

Due to a defect in the renal tubules resulting in renal insensitivity to ADH
-familial X-linked trait
-Acquired due to pyelonephritis, K+ depletion, sickle cell anemia, chronic hypercalcemia, medications (e.g. lithium, methicillin, etc)

102
Q

DI: S/Sx

A

thirst/cravings for water (fluid intake 5-20 L/day)
Polyuria (2-20L/day) and nocturia
Weight loss
Fatigue
Changes in LOC
Dizziness
Elevated temperature
Tachycardia
Hypotension
Poor skin turgor, dry mucous membranes

103
Q

DI: labs/Dx

A

Hypernatremia
Elevated BUN/Cr (BUN fluctuates d/t dehydration)
Serum osmolality >290 mOsm/kg
Urine osmolality <100 mOsm/kg
Urine spec grav low <1.005

Vasopressin (Desmopressin) challenge test - 0.05-0.1 ml nasally or 1 ug SQ or IV with measurement of urine volume
-Central DI: positive
-Nephrogenic DI: negative

If no apparent cause, MRI to rule out mass/lesion

104
Q

DI: management

A

IV fluids:
- Na+ >150: give D5W to replace half of volume deficit in 12-24 hrs (rapid lowering of Na+ can cause cerebral edema)
- When Na+ <150, switch to 1/2NS or NS

DDAVP 1-4 mcg IV/SQ every 12-24 hours for acute situations
- Maintenance dose of DDAVP is 10 ug Q12-24 hrs intranasally

105
Q

How to evaluate for primary aldosteronism

A

Hold diuretics
Add 1 teaspoon of salt to daily diet for 5 days, then collect 24-hour urine sample for creatinine, sodium, and aldosterone to determine if elevated aldosterone is secondary to dietary salt restriction

106
Q

primary aldosteronism: essential feature

A

elevated and inappropriate aldosterone

107
Q

acromegaly

A

clinical syndrome that occurs as a result of excessive growth hormone secretion

108
Q

acromegaly: clinical findings/ presentation

A

growth stimulation in connective tissue, cartilage, bone, skin
thickening of skin and coarse facial tissues
enlarged thyroid with/without hyperthyroidism
LVH, cardiomyopathy
hypertension
sleep apnea
adult onset

109
Q

Which drugs can block or mask early signs of hypoglycemia

A

beta blockers

110
Q

target A1c for patients >65 years old with significant comorbidities

A

<8.0%

Comorbidities:
-cancer
-CHF
-depression
-falls
-HTN
-stage 3 or worse CKD
-stroke

111
Q

Earliest marker for diabetic nephropathy

A

microalbumin
can be detected before the patient is symptomatic
-Gold standard: urine albumin concentration from an early morning urine sample

112
Q

When to discontinue metformin in a patient with CKD

A

GFR <30 mL/min (risk of lactic acidosis)

113
Q

Oral hypoglycemic agent that should be avoided in elderly patients due to susceptibility to dehydration and AKI, and thus hypoglycemia

A

sulfonylureas (glyburide)

114
Q

When transitioning from an insulin infusion to subcutaneous basal insulin, when should you stop the insulin drip?

A

1-2 hours after the basal insulin is given

Anion gap should be normal to <12 mEq/L

115
Q

How to manage insulin while a patient is NPO and hyperglycemic

A

Long acting insulin
Correctional (basal) insulin
Hold prandial insulin

Board Exam (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions