endocrine Flashcards
diabetes mellitus: pathophysiology
metabolic disease
- inability to produce/utilize insulin = causes hyperglycemia
diabetes type 1: pathophys
total DESTRUCTION of beta cells; thought to result from infectious/toxic environmental insult to beta cells in genetically prediposed
- d/t islet cell antibodies found in 90% w/in 1 year
- ketone development occurs
Insulin DEPENDENT.
DM1: s/s
P olyphagia
P olydypsia
P olyuria
W eight loss
diabetes mellitus (either 1 or 2): diagnostics x5
- random BG: gt 200 mg/dL (+ uria/dips/wt loss)
- fasting BG: gt 126 mg/dL x2 diff occasions
- HgbA1c: gt 7%
- ↑ ↑ BUN/Cr d/t dehydration
- DM1 only: ketonemia/uria
What pharmacological therapy is indicated if patient presents with ketones and DM1?
insulin therapy @ 0.5 units/kg/day
split: give ⅔ AM & ⅓ PM
What are the Conventional Split Dose Mixtures of insulin administration for DM1?
AM: ⅔ NPH; + ⅓ Regular
PM: ½ NPH + ½ Regular
What are 3 insulin analogs?
RAPID ACTING
aspart (NovoLog)
lispro (Humalog): rapid onset
LONG-ACTING
glargine (Lantus): prolonged duration
DM2: pathophysiology
circulating insulin insufficient to meet body’s needs but IS enough to prevent ketoacidosis
causes:
- tissue insensitivity
- insulin secretion defect leading to resistance and/or impaired insulin production
What are the diagnostic criteria for Metabolic Syndrome?
3+ of... WAIST: M 40+ & F 35+ BP: over 130/85 TRIGS: 150+ FBG: 100+ HDL: less than 40(M) or 50(F)
40 yo. F presents to ED with complaints of four UTIs in the past 6 months and chronic skin infection with increasing pruritus. What is most likely differential?
DM Type II. Women often first present with recurring vaginitis, plus chronic skin infections are associated with DM2.
What is the initial therapy indicated for DM Type II management? x3
weight loss (obese pts)
consider early use of oral agent
dietary tx & exercise
What pharmacological intervention is considered the standard of care upon diagnosis of DM2?
metformin (Glucophage)
What is a major AE of metformin (Glucophage)?
LACTIC ACIDOSIS
If patient complains of muscle cramps/pain - think LA.
glipizide (Glucotrol)
glyburide (Diabeta)
glimepiride (Amaryl)
These fall in what class? What is the mechanism of action?
diabetic oral agents: sulfonylureas
MOA: stimulate pancreas to release more insulin
A key feature of DM Type II is Metabolic Syndrome. To make this diagnosis, you need three of the following EXCEPT:
a. Waist circumference M 40, F 35
b. BP 140/90
c. Fasting BG t100
d. HDL M 40, F 50
B. The BP in Metabolic Syndrome is greater than 135/85.
What is the function of incretins in diabetes pathophysiology?
incretins signal pancreas to increase insulin secretion and liver to stop producing glucagon
60 yo. F with PMH significant for DM Type II is being discharged. Lipid acting drug therapy should be especially considered for this patient with the following:
a. triglycerides 140
b. HDL 40
c. cholesterol 200
d. LDL 90
D. Goal LDL is less than 60
What is the Somogyi Effect?
Nocturnal hypoglycemia stimulates surge of counter regulatory hormones that raise blood sugar. Hypoglycemia @ 0300 results in rebound causing hyperglycemia @ 0700
SOMOGYI SURGE
What is the treatment for Somogyi Effect?
reduce /omit bedtime dose of insulin
What is the Dawn Phenomenon?
Tissue DESENSITIZED to insulin nocturnally. BG progressively elevates through night resulting in hyperglycemia @ 0700.
DAWN IS RISING
What is the treatment for Dawn Phenomenon?
add/increase bedtime dose of insulin
DKA: pathophysiology
intracellular dehydration as a result of hyperglycemia, often acute complication of DM1 (may be presenting sign)
DKA: hallmark s/s x6
Kussmaul breathing
altered LOC
fruity breath
dehydration - poor skin turgor, orthostatic hypotension with tachycardia
DKA: diagnostics x6
BG over 250 mg/dL keton-emia/-uria metabolic acidosis: pH less than 7.3 + ↑AG hyperkalemia leukocytosis hyperosmolality
DKA: mgmt x7
- protect airway; oxygen
- 1st hour: min 1L NS IVF then 500 mL/hr
- if glucose 500+ use ½NS after 1st hr (water exceeds Na loss)
- when glucose under 250 give D5 ½NS (prevent hypoglycemia)
- 0.1u/kg regular insulin IV bolus then 0.1u/kg/hr
- if glucose doesn’t fall after 1 hr, repeat bolus
- severe acidosis lt 7.1: correct w bicarb drip (44-48mEq in 900 mL ½NS) until gt 7.1
- do not treat initial hyperkalemia
- UOP monitored hourly
- supportive
HHNK: pathophysiology
also intracellular dehydration d/t elevated blood glucose
- usually complication of DM2
- insulin production impaired, not sufficient to prevent severe hyperglycemia, osmotic diuresis, extracellular fluid depletion.
HHNK: hallmark s/s
NO KETONES IN URINE!
- dehydration (poor turgor, tachycardia, orthostatic hypotension)
- changes in LOC
HHNK: diagnostics x4
- BG gt 600 mg/dL; often 1000+
- hyperosm: gt 310 mOsm/L
- ↑ ↑ BUN/Cr r/t dehydration
- NORMAL pH & anion gap + NO KETONES
HHNK: mgmt x4
- protect airway; O2.
- fluid deficit 6 - 10L: massive fluid replacement, NS IVF then ½NS then D5½NS
- 15u regular insulin IV bolus followed by 10 - 15u SQ STAT (additional insulin depends on severity/response)
- supportive care
hyperthyroidism: classic s/s
↑ sweating, smooth/warm/moist skin tachycardia, a fib hyperthermia/heat intolerance weight loss exopthalmos emotional lability, fatigue hyperreflexia thinning hair
What is the most sensitive test in diagnosing hyperthyroidism?
TSH assay
Hyperthyroidism: ↓TSH + ↑T3
hyperthyroidism: T3
↓T3 (80 - 230 ng/dL)
A low thyroid radioactive iodine uptake is associated with what etiology of hyperthyroidism?
subacute thyroiditis
What is the pharmacological management of a patient with small goiter; mild cases of hyperthyroidism; or fear of isotopes?
Thiourea drugs
Methimazole (Tapazole) 30-60 mg TID daily
Propulthiouracil 300-600 mg QID daily
What drug class is used for symptomatic relief in hyperthyroidism?
Beta Blockers - Propanolol (Inderal) 10 mg PO and titrate up to max 80 mg PO QID daily.
What is used to destroy goiters in hyperthyroidism?
Radioactive iodine-131
What medication is contraindicated during a thyroid crisis and why?
ASA - it can exacerbate storm.
What is the most common cause of hypothyroidism?
Hashimoto’s thyroiditis
hypothyroidism: hallmark s/s
extreme weakness, arthralgias, cramps cold intolerance weight gain edematous hands, face constipation dry skin, hair loss, brittle nails
hypothyroidism: TSH presentation assay
↑ TSH, ↓ T4
T3 is not a reliable test
In addition to TSH assay, what two lab values are of note when diagnosing hypothyroidism?
Hyponatremia
Hypoglycemia
What pharmaceutical intervention is the standard of care in treating hypothyroidism?
levothyroxine (Synthroid) 50 - 100 mcg QD
- ↑ dose 25 mcg QD for 1 - 2 wks until stable
- elderly: start low go slow
- @ 60, decrease dose
Considerations for levothyroxine in older adults? x2
60+ = decrease dose
if new dx, start low & go slow
What lab value is used to monitor the effectiveness of levothyroxine (Synthroid)?
TSH
What AE is most responsible for decreased compliance with levothyroxine (Synthroid)?
Alopecia. Hair falls out in clumps - it is temporary but distressing.
What is the most common cause of hyponatremia?
Hyperglycemia (as with HHNK).
What is Cushing’s Syndrome and what are 3 causes?
Adrenal glands gone haywire. THINK: TOO MUCH STEROID
ACTH hypersecretion by pituitary
Adrenal tumor
Chronic glucocorticoid use
Cushing’s Syndrome: hallmark s/s
moon face, buffalo hump, central obesity hypertension acne, purple striae, poor wound healing/freq infection hirsutism amenorrhea, impotence
Which 2 adrenal-related labs are elevated in Cushing’s Disease?
AM cortisol
Serum ACTH
Cushing’s Syndrome: glucose, Na, K
hyperglycemia
hypernatremia
hypokalemia
Cushing’s Syndrome: mgmt x5
DEPENDS ON CAUSE!
- d/c glucocorticoids
- transphenoidal resection of pituitary adenoma
- resection of ACTH secreting or adrenal tumors
- manage electrolyte imbalance
Addison’s Disease: pathophysiology
adrenal insufficiency ∴ deficiency in androgens, cortisol, aldosterone
Addison’s Disease: hallmark s/s
hyperpigmentation: buccal mucosa & skin creases (nipples, nail beds, knuckles, palms, neck) diffuse tanning/freckles orthostasis, hypotension scant axillary, pubic hair acute: fever, worsening of sx, Δ LOC
Addison’s Disease: glucose, Na, K
hypoglycemia
hyponatremia
hyperkalemia
What lab is ordered to rule out Addison’s Disease?
Cosytropin - measures how well adrenal glands respond to ACTH
Addison’s Disease: outpatient mgmt x3
- specialist referral
- replace glucocorticoid (hydrocortisone) & mineralcorticoid (fludrocortisone)
SIADH: pathophys
release of ADH occurs independent of osmolality or volume-dependent stimulation
INAPPROPRIATE WATER RETENTION
SIADH: hallmark s/s
neuro changes r/t hyponatremia: HA, seizures, coma
weight gain/edema
↓ UOP
SIADH: diagnostics
hyponatremia but EUVOLEMIC
* ↓ serum osm lt 280
* ↑ urine osm gt 100
urine Na gt 20
Patient has been diagnosed with SIADH with serum Na gt 120 mEq/L. Treatment plan?
restrict total fluids to 1000 mL/24 hrs
Patient has been diagnosed with SIADH and is having neuro symptoms with serum Na less than 110 mEq/L. Treatment plan? x3
can use iso or hyper: NS or 3% NS IVF - SLOW admin
+ furosemide (Lasix) 1 - 2 mEq/hr.
monitor Na/K losses hourly + replete as needed
Patient has been diagnosed with SIADH, has no neuro symptoms, and has serum Na 115 mEq/L. Treatment plan? x2
restrict fluids to 500 mL/24hrs
monitor
What is central diabetes insipidus and what are the causes x4?
pituitary or hypothalamus damage → ADH deficiency
causes:
- surgical damage
- trauma
- infection
- metastatic carcinoma
What is nephrogenic diabetes insipidus and what are the causes x5?
renal tubule defect → renal insensitivity to ADH
causes:
- familial X-linked
- pyelonephritis
- K depletion
- sickle cell anemia
- meds
diabetes insipidus: hallmark s/s
thirst, fluid intake: 5 - 20 L/day polyuria: 6 - 20 L/day nocturia tachycardia, hypotension, dizziness AMS, fatigue weight loss, poor turgor
diabetes insipidus: diagnostics x5
hypernatremia
↑ serum osm gt 290
↑ BUN/Cr
these two go together;
- ↓ urine osm lt 100
- ↓ urine specific gravity lt 1.005
Patient has diabetes insipidus and serum Na of gt 150 mEq/L. Treatment plan?
Give D5W IV to replace 1/2 FVD in 12-24 hours
What is a major complication associated with rapid lowering of serum sodium?
Cerebral edema.
diabetes insipidus: acute mgmt
DDAVP 1-4 ug IV or SQ q 12-24 hrs
diabetes insipidusL maintenance treatment
maintenance dose: DDAVP 10 ug q 12-24 hrs INTRANASALLY
pheochromocytoma: pathophys
excess catecholamine (epi + NE) release characterized by paroxysmal or sustained HTN
most commonly caused by TUMOR of the adrenal MEDULLA
Pheochromocytoma is often associated with what hallmark symptom?
Labile HTN and postural hypotension
** What are the four components of the urine assay that is diagnostic for a pheochromocytoma? **
!!!!
urine catecholimines
metanephrines
vanillylmandelic acid (VMA)
creatinine
What diagnostic confirms a pheochromocytoma?
adrenals CT to confirm and localize tumor
Expected TSH value given pheochromocytoma?
The TSH is normal with a pheo.
What is the treatment of choice for pheochromocytoma?
surgical removal of adrenal medulla tumor
What are 3 possible complications that should be monitored in patients who are s/p surgical removal of tumor that was causing pheochromocytoma?
hypotension (r/t depleted catecholamines)
adrenal Insufficiency
hemorrhage
The most common complication associated with diabetes is:
retinopathy
What is the most prevalent risk factor for type II DM?
Obesity
The two most common causes of hypercalcemia are:
Malignancy
Hyperparathyroidism
Metabolic abnormalities seen in Addison’s Disease include:
- hyponatremia s/t renal tubular loss of sodium ions
- hyperkalemia s/t decrease in cortisol which helps to regulate intracellular and extracellular potassium and sodium
- hypoglycemia
Metabolic Acidosis
30 yo. D with PMH of DM Type II is scheduled for a cardiac cath within the next 7 days. Home medications include Metformin (Glucophage) 500 mg TID. What instructions would you give her regarding her medications?
Instruct the patient to stop Metformin (Glucophage) at least 3 days before procedure. The use of Metformin (Glucophage) and contrast dye could cause ARF.
A patient with DM and HTN should be on which classification of medication and why?
ACE Inhibitors - to reduce proteinuria and the resulting diabetic nephropathy
HgbA1C: normal range + good control
normal 5.5 - 7
good control @ 6 (given DM)
impaired glucose tolerance values
FBG 100 - 125
1 reason for BUN fluctuation?
dehydration
normal range BUN & Cr?
10 - 20 & 0.5 - 1.5
lispro (Humalog): very important admin consideration
lispro (Humalog) has very rapid onset, must give food with it otherwise hypoglycemia will occur within 5 - 10 minutes
What is intensive therapy of insulin for DM1?
reduce/omit PM dose and add at bedtime
As waist circumference increases, risk for what increases?
risk of sudden cardioembolic death - above Metabolic Syndrome thresholds, this risk is substantive
What is the most widely prescribed oral antidiabetic?
sulfonylureas
What class of meds can be used as an adjunct to sulfonylureas but can also be used alone? When would you use it alone?
biguanides (metformin)
use alone for obese pts
DKA vs HHNK
DKA / HHNK DM1 / DM2 BG 250+ / 600 - 1000+ metabolic acidosis / normal anion gap ketones / none
What diagnostic test is performed to establish etiology of hyperthyroidism?
thyroid radioactive iodine uptake
A high thyroid radioactive iodine uptake is associated with what etiology of hyperthyroidism?
Grave’s Disease
normals: TSH Total T4 Free T4 T3
TSH: 0.4 - 5.0
Tot T4: 4.5 - 11.5
Free T4: 0.8 - 2.8
T3: 75 - 200
Most common presentation of hyperthyroidism?
Grave’s Disease
5 potential causes of hyperthyroidism
Grave's Disease subacute thyroiditis toxic adenoma TSH secreting pituitary tumor high dose amiodarone
What cardiac med has the potential AE of hyperthyroidism?
amiodarone (at high doses)
6 causes of hypothyroidism
Hashimoto's thyroiditis pituitary TSH deficiency hypothalamic TRH deficiency iodine deficiency gland damage idiopathic
hyperthyroidism: mgmt
- refer to specialist esp w comorbs
- propranolol (Inderal): sx relief - begin @ 10mg up to 80mg QID; subacute thyroiditis best treated symptomatically with this
- radioactive iodine 131-I: destroy goiter
- thyroid surgery
- lugol’s solution: reduce gland vascularity, 2 - 3 gtt PO QD x10 days
- thiourea drugs: mild cases, small goiter, or isotope aversion
- methimazole (Tapazole): 30 - 60mg QD across 3 doses
- propylthiouracil 300 - 600mg QD across 4 doses
Thyroid disease indication + use for propranolol (Inderal)?
symptomatic relief for hyperthyroidism, also, subacute thyroiditis best treated symptomatically with it
begin @ 10mg up to 80mg QID;
Thyroid disease indication + use for lugol’s solution?
in hyperthyroidism to reduce gland vascularity, 2 - 3 gtt PO QD x10 days
Thyroid disease indication + use + 2 examples of thiourea drugs?
mild cases of hyperthyroidism or with small goiters, or patient refuses isotope
methimazole (Tapazole): 30 - 60mg QD across 3 doses
propylthiouracil 300 - 600mg QD across 4 doses
thyroid storm: mgmt
propylthiouracil 150 - 250 g q6 hours
OR
methimazole (Tapazole) 15 - 25mg q6 hrs PLUS the following in 1 hour:
- Lugol’s Sol’n 10 gtts TID
OR
- Na iodide 1g slow IV PLUS the following:
– propranolol 0.5 - 2g IV q4 hrs or 20 - 120 mg PO q6 hrs WITH
– hydrocortisone 50 mg q6 hrs with rapid reduction as situation improves
myxedema coma: what is it + mgmt x6
hypothyroid crisis
- protect airway (vent if needed)
- fluid replacement
- levothyroxine 400 mcg IV once, then 100 mcg QD
- hypotension support
- slow rewarming with blankets to avoid circulatory collapse
- symptomatic care
What is the dosage of levothyroxine in a myxedema coma?
IV !!!!!!!
levothyroxine 400 mcg IV once
THEN
100 mcg QD
Why do you see hypertension in Cushing’s Syndrome?
steroids induce vasoconstriction
What 2 adrenal-related labs can be seen in Addison’s Disease?
↓↓ plasma cortisol: less than 5 mcg/dL @ 0800
cosyntropin test
Addison’s Disease x4
autoimmune destruction of adrenals
bilateral adrenal hemorrhage (ex: w anticoag tx)
pituitary failure = ↓ ACTH
metastatic cancer
Cushing’s vs Addison’s: glucose, Na, K
CUSHY:
hypergly, hyperNa, hypoK
ADDY:
hypogly, hypoNa, hyperK
Addison’s Disease: inpatient mgmt
hydrocorisone (Solu-Cortef) 100 - 300 mg IV initially w NS
- replace volume with D5NS at 500 cc/hr x4 hours then taper as appropriate
- vasopressors usually ineffective
TREAT THE UNDERLYING CAUSE! (Often infection, sepsis)
What is often the underlying cause for Addison’s Disease?
infection - sepsis
What is usually ineffective in the treatment of Addison’s Disease requiring hospitalization?
vasopressors
The symptoms of SIADH are largely related to what imbalance?
hyponatremia
SIADH: mgmt for 3 different levels of acuity
serum Na gt 120
- restrict water to 1000 mL/24 hrs + monitor
serum Na 110 - 120 & no neuro symptoms
- restrict water to 500 mL/24 hrs + monitor
neuro symptoms +/- serum Na lt 120
- NS or 3%NS SLOWLY
- furosemide 1 - 2 mEq/h
- monitor Na/K losses hourly & replete
urine specific gravity normal
1.010 - 1.030
What is a vasopressin (Desmopressin) challenge test and when is it used?
use if central diabetes insipidus is suspected
give 0.05 - 0.1 mL nasally
OR
1 ug SQ or IV & measure urine volume
POSITIVE in central DI
NEGATIVE in nephrogenic DI
diabetes insipidus mgmt x 2 serum levels + acute + maintenance
serum Na 150+ give D5W** to replace ½ volume deficit in 12 - 24 hrs (SLOWWW)
serum Na under 150: give ½ or NS
acute: DDAVP 1 - 4 ug IV or SQ q 12 - 24 hrs
maintenance DDAVP: 10 ug q 12 - 24 hrs intranasally**
pheochromocytoma: diagnostic process x4
TSH: if normal…
then check
- plasma-free metanephrines
- assay of urine catecholamines
then CT of adrenal glands: confirms & localizes tumor
What is important to r/o if you suspect pheochromocytoma? How do you rule it out x3?
hyperthyroidism! r/o with
TSH level
observation of labile hypertension and postural hypotension
in suspected pheochromocytoma, 24 hour urine test expected findings **
2.2+ ug metanephrine / mg creat
AND
5.5+ ug VMA / mg creat
MICROGRAMS OF METANEPHRINE AND VMA
