Diabetes Mellitus Flashcards

(208 cards)

1
Q

What is Type 1 diabetes?

A

Deficiency of insulin SECRETION

Absolute lack of secretion

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2
Q

What is Type 2 diabetes?

A

Combo of insulin RESISTANCE and inadequate SECRETION to compensate for the resistance
Relative insulin deficiency

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3
Q

What is Prediabetes?

A

Impaired fasting glucose

impaired glucose tolerance

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4
Q

Highest incidence of diabetes is in the…

A

American Indian/Alaska native population

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5
Q

There is a strong genetic component in…

A

Diabetes Type 1

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6
Q

Obesity and visceral abdominal fat is a risk factor for…

A

Type 2 diabetes

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7
Q

Type 2 diabetes causes…

A

Accelerated gastric emptying
Excess hepatic glucose production
Defective uptake of glucose in the muscles
Defective insulin secretion

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8
Q

Clinical manifestations of type 1 diabetes…

A
Polyuria
Polydipsia
Polyphagia
Blurred Vision
Weight loss
Muscle catabolism
Paresthesia
DKA typically is their presenting factor
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9
Q

Clinical manifestations of type 2 diabetes…

A
Initially asymptomatic
polyuria
polydipsia
polyphasic
skin infections
pruritus
Vaginitis (fungal)
Overweight/obese
acanthuses nigricans- dark spots in skin folds
HHNK- rare presenting factor
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10
Q

Polysdipsia, polyuria is caused by…

A

osmotic diuresis secondary to hyperglycemia and dumping of glucose in the urine

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11
Q
Screening for type 2 diabetes. 
Consider testing (2018 recommendations)...
A
  • Informal assessment of risk factors in all patients
  • In asymptomatic adults with BMI > 25
  • Asian americans with BMI > 23 who have 1 or more additional DM risk factors
  • Yearly testing of pre diabetes patients, if normal then test every 3 years
  • ALL patients over the age of 45
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12
Q

Screening for type 2 diabetes diagnostics should include…

A
  • Fasting Plasma Glucose
  • 2 hour plasma glucose
  • Hemoglobin A1C
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13
Q

Who should be screened for type 2 diabetes?

A
A1C > 5.7%
First degree relative with diabetes
High risk race/ethnicity (AA, Latino, Native American, Asian, Pacific islander)
Women diagnosed with gestational diabetes
History of CVD
HTN
HDL
Women with PCOS
Physical inactivity
Severe obesity
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14
Q

Diagnostic criteria for Type 2 diabetes…

A

Plasma glucose > 126 on more than one occasion after 8 hour fast
> 200 random glucose
Fasting BG 100-125 - proceed to oral glucose tolerance test
OGTT 2 hour value of > 140-199 (IGT)
OGTT > 200
HbA1C > 6.5 - gold standard for diagnosis

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15
Q

How to perform an oral glucose tolerance test…

A

Drink 75 mg glucose in 300 cc H2O within 5 minutes
Perform in the AM
No smoking or activity during the test
Obtain samples 0-120 minutes

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16
Q

The gold standard for diagnosis of type 2 diabetes is…

A

HbA1c

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17
Q

HbA1C is not accurate in…

A
pregnancy
increased red blood cell turnover
sickle cell disease
hemodialysis
recent blood loss or transfusion
Epo therapy
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18
Q

Pre-diabetes diagnostic values…

A

FPG 100-125
2 hour glucose (140-199)
HbA1C 5.7-6.4

Implement lifestyle changes

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19
Q

Additional labs needed in patients with pre-diabetes or diabetes

A
Fasting lipid
LFT
Urinary albumin-creatinine ration
creatinine, GFR
TSH
Microalbuminuria
ECG
Urinalysis (ketone, protein, sediment)
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20
Q

High TSH

Decreased TSH

A

Decreased insulin production and utilization

High insulin production and utilization

Higher incidence of thyroid disfunction in patients with diabetes.

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21
Q

The preferred initial pharmacologic agent for Type 2 DM is…

A

Metformin

Monitor Vitamin B 12 periodically

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22
Q

Consider insulin if for initial managment of type 2 DM if…

A

symptomatic
elevated BG levels > 300
HbA1c > 10

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23
Q

Start a second oral agent, a GLP-1 receptor agonist or basal insulin if…

A

non insulin mono therapy is at the maximal tolerated dose and does not achieve or maintain the A1C target over 3 months.

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24
Q

Treatment of patients with T2DM and ASCVD should be..

A

lifestyle management
metformin
then subsequently incorporate an agent proven to reduce major adverse CV events such as: empagliflozin and liraglutide
Can also consider canagliflozin

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25
At diagnosis if A1C is less than 9% then consider...
monotherapy | lifestyle changes + metformin
26
At diagnosis if A1c is greater than or equal to 9 then consider...
dual therapy (lifestyle changes + metformin + additional agent) Additional agent is determined based on if the patient has ASCVD or not
27
If patient on dual therapy and A1C is not at target after 3 months then consider...
triple therapy | lifestyle management, metformin, and two additional agents
28
If A1C is > 10 or BG is greater than 300 then consider...
combination injectable therapies.
29
Biguanides: Metformin | MOA
Acts on liver- decrease glucose production, muscle, and adipose- increased uptake
30
Biguanides contraindications
Cr > 1.4 in women or 1.5 in men hepatic failure alcoholism
31
Biguanides dosage range
500-2000 mg daily
32
Biguanides major side effects
GI upset lactic acidosis B-12 deficiency AKI
33
How is glycemic control monitored?
Perform A1C 2x annually in patients that meet treatment goals Perform A1C quarterly in patients whose therapy has changed or who are not meeting their treatment goals.
34
What lifestyle modifications should be introduced?
``` Nutrition therapy limit alcohol intake sodium restriction 150 min/week of physical activity Stop tobacco products psychosocial care metformin therapy for prevention of diabetes in those with pre diabetes. ```
35
Sulfonylureas are...
glimepiride glipizide glyburide
36
MOA of sulfonylureas...
Stimulate voltage gated calcium channels act on pancreatic B cells to promote insulin release. Metabolized in liver excreted in kidneys
37
Sulfonylureas contraindications
severe renal impairment hepatic failure caution with CV disease and elderly
38
Major side effects of sulfonylureas
Hypoglycemia
39
Meglitinide analogs MOA
Only difference from sulfonylureas is that they don't stimulate voltage gated calcium channels, still block Potassium channels Excreted in bile Pulses of insulin from pancreatic B cells
40
Name of meglitidine analog
Repaglinide
41
Meglitinide analog contraindications
Use with caution with other CYP450 medications
42
Major side effects of Meglitinide analogs
Hypoglycemia
43
Dosing for Meglitinide analog
Give 15 minutes before meals, can combine with metformin appropriate for renal impairment and elderly Can be used as an initial therapy for those with contraindications to metformin
44
D-Phenylalanine derivatives
Nateglinide
45
D-P D MOA
Binds to sulfonylurea receptors absorbed in intestines metabolized by liver results in rapid pulses of insulin
46
DPD dosing
Appropriate for patients with renal impairment and elderly given pre meal may be combined with metformin
47
Thiazolidinediones
Pioglitazone (actos) | Rosiglitazone (Amanda)
48
Thiazolidinediones MOA
sensitizes peripheral tissue to insulin | metabolized by the liver
49
Thiazolidinediones Contraindications
Cardiovascular disease
50
Thiazolidinediones Side effects
``` Angina, AMI (avandia) Edema Fractures (decreases bone density) Anemia Weight gain (sodium reabsorption) ```
51
Thiazolidinediones dosing
May be combined with sulfonylureas or metformin
52
Alpha-glucosidase inhibitors
Acarbose | Miglitol
53
Alpha-glucosidase inhibitors MOA
Slow absorption of carbohydrates in the upper GI tract | Reduces postprandial glucose surge
54
Alpha-glucosidase inhibitors contraindications
Avoid in CKD
55
Alpha-glucosidase inhibitors side effects
flatulence risk of hypoglycemia with sulfonylureas elevated LFTs
56
Alpha-glucosidase inhibitors dosing
Give with the first bite of food
57
GLP-1 receptor agonists
Byetta- weekly Victoza Trulicity-weekly
58
GLP-1 MOA
"Incretins" Enhance glucose stimulated insulin secretion Suppress glucagon production Delay gastric emptying May lead to weight loss and appetite suppression
59
GLP-1 Contraindications
Medullary thyroid cancer | Multiple endocrine neoplasia
60
GLP-1 Major side effects
N/V/D | Increased risk for thyroid cancer
61
GLP-1 Dosing
Injectable | May be combined with metformin, sulfonylureas or TZDs
62
DPP-4 inhibitors
Onglyza Januvia Tradjenta
63
DPP-4 inhibitors MOA
"incretins" Do not combine with GLP-1 Inhibit the degradation of GLP-1 Increased effect on post-prandial glucose
64
DPP-4 inhibitors contraindications
CKD
65
DPP-4 inhibitors Major side effects
Hypersensitivity reactions Stevens-Johnson syndrome Possible pancreatic effects Joint pain
66
DPP-4 dosing
Reduce in patients with renal impairment Can be combined with Metformin, sulfonylureas and TZDs Can decrease albuminuria Steer clear with CHF patients
67
SGLT-2 inhibitor
Invokana (ASCVD) Farxiga Jardiance (ASCVD- decreases mortality)
68
SGLT-2 MOA
Increases urinary glucose excretion by preventing reabsorption in the kidneys
69
SGLT-2 contraindications
Moderate renal insufficiency
70
SGLT-2 major side effects
UTI Vaginitis Dehydration
71
SGLT-2 dosing
Farxiga- reduce dosing with hepatic impairment
72
Initiate basal insulin at...
10 u/day or 0.1-0.2 u/kg/day Increase by 10-15% or 2-4 unites once or twice weekly until you reach FBG target For hypoglycemia: determine & address cause, if no clear cause then decrease by 4 units or 10-20%.
73
Treatment for Type 1 DM should be ...
Treated with multiple daily injections of prandial insulin and basal insulin OR a continuous subcutaneous insulin infusion
74
What is an amylin analog that has been approved for T1DM
Pramlintide
75
Rapid acting insulin pharmacokinetics | Lispro-humalog, Aspart- novolog, Glulisine- Apidra
Starts to work in 15-30 minutes Peak 1-2 hours Duration 3-6 hours Maximum duration 4-6 hours
76
Short acting insulin pharmacokinetics | regular
Starts to work in 30 min-1 hour Peak action- 2-4 hours Duration- 3-6 hours Max duration 6-8 hours
77
Intermediate acting insulin pharmacokinetics | NPH
Starts to work in 2-4 hours Peak 8-10 hours Duration 10-18 hours Max duration 14-20 hours
78
Long acting insulin | Glargine- Lantus
Starts to work in 1-2 hours No peak Duration 19-24 hours Max 24 hours
79
Long acting insulin | Detemir- Levemir
Starts to work in 1-2 hours No peak Duration 19-20 hours Max- 20 hours
80
T1DM insulin regimens
0.5 u/kg/day 2/3 AM 1/3 PM
81
Physiologic regimen
Basal long acting (1/3) + pre meal bolus (2/3)
82
Conventional split dose regimen
AM: NPH (2/3) + Regular (1/3) PM: NPH (1/2) + Regular (1/2) Prandial- insulin analog based on CHO intake
83
Continuous Subq Insulin infusion
Hourly basal rate (1/2) + Prandial bolus (1/2)
84
What is somogyi effect?
Nocturnal hypoglycemia then hyperglycemia by 0700 | Treatment: Bedtime snack
85
What is the dawn phenomenon
Nocturnal decrease in insulin sensitivity leading to hyperglycemia by 0700 Treatment: increase evening insulin dose
86
Complications of insulin therapy
Hypoglycemia Financial burdens QOL demands behavioral changes
87
Cardiovascular complications of DM screening
``` All patients with DM should have CV risk factors assessed annually Dyslipidemia HTN Smoking Family Hx Assess urine for albuminuria ```
88
The leading cause of morbidity and mortality in DM patients is
Cardiovascular complications
89
For patients with increased risk of CV disease | Who are they and what is recommended?
Patients over the age of 50 who have at least one additional risk factor Or if they are < 50 but with multiple other risk factors clinical judgement required aspirin therapy 75-162 mg/day
90
For patients with CV risk factors and ASA allergy, use...
Plavix
91
Patients with DM and HTN should be treated to a blood pressure goal of less than... Treatment:
<130 systolic (<140 ADA) <80 diastolic (<90 ADA) They should be treated with lifestyle and pharmacologic therapy ACE or ARB is first line therapy May use Thiazides and dihydropyridine CCBs
92
Lipid management and DM screening should be..
At diagnosis At initial medical evaluation Every 5 years or more if indicated
93
CAD and DM screening recommendations
``` If asymptomatic, routine screening is not recommended. Consider investigations with... Atypical symptoms s/s of associated vascular disease EKG abnormalities ```
94
Treatment of CAD and DM in patients with known ASCVD...
use ASA and statin therapy and consider ACE | With prior MI continue BB for at least 2 years
95
Nephropathy and DM screening...
at least once a year by assessing urinary albumin and eGFR All patients with T1DM > 5 years All patients with T2DM All patient with comorbid HTN
96
Nephropathy and DM treatment...
BG control BP control ACE/ARB not recommended for primary prevention in patients with normal BP eGFR < 30- consult for evaluation for RRT
97
Retinopathy and DM screening...
Dilated and comprehensive eye exam: T1DM within 5 years of onset T2DM at time of diagnosis ``` Manifestations of diabetic retinopathy include: hard exudates Fovea Microaneurysms Hemorrhages Cotton wool spots ```
98
Neuropathy and DM screening..
T1DM 5 years T2DM at diagnosis ``` Should include 10g monofilament testing vibration sensation temperature pinprick ```
99
Treatment for neuropathy...
BG control Treat for pain with pregabalin, Neurontin, duloxetine
100
Foot care for DM...
Comprehensive foot evaluation annually Feet inspected every visit Examine skin, foot deformities, neurologic assessment, vascular assessment
101
Inpatient care for patient with DM
perform hbA1c on all patients Insulin therapy initiated for BG > 180 Sole use of SS insulin in inpatient is strongly discouraged Tailor discharge plan to patient Have a hypoglycemia management protocol in place
102
Management of surgical patients with DM...
*
103
Mechanism of negative feedback loop for thyroid...
Hypothalamus secretes thyroid releasing hormone (TRH) which acts on the anterior pituitary which then releases thyroid secreting hormone (TSH) which stimulates the release of hormones T3, T4 from he thyroid. T3, T4 have a negative response on the pituitary and hypothalamus to stop releasing their hormones if there is enough.
104
If we have a decrease T3, T4 then there will be an increase in the production of...
TRH, TSH (both high) Hypothyroid
105
Elevated levels of T3, T4 then there is a negative feedback there will be a decrease in the production of ....
TRH, TSH (both low) Hyperthyroid
106
Clinical manifestations of hypothyroid...
``` Fatigue, weakness cold intolerance dyspnea on exertion weight gain cognitive dysfunction constipation decreased hearing depression myalgia menorrhagia arthralgia dry skin hoarseness edema bradycardia slow movement/speech ```
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Who should be screened for hypothyroid...
``` All patients with clinical s/s Presence of a goiter History of autoimmune disease Head/neck irradiation Family history Meds that could interfere HLD Hyponatremia Anemia Pericardial/pleural effusions Pituitary pathology ```
108
What tests are used to diagnose hypothyroid...
TSH "gold standard"- elevated with primary hypothyroidism Free T4 ``` Additional testing: Lipid Blood glucose Sodium CBC (normocytic or microcytic anemia) Antithyroglobulin Ab Antithyroperoxidase Ab CT/MRI neck for goiter ```
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What are the normal thyroid lab values
TSH 0.5-4 | Free T4- 4.6-12
110
Hypothyroid treatment...
Levothyroxine 25-75 mpg/day (young adults) 50 mpg/day (older adults) repeat TSH in 8 weeks titrate dosage to clinical s/sx and repeated labs careful not to induce hyperthyroid increase at 25 mcg increments Then repeat blood work annually when on a set dose
111
Common clinical presentations of myxedema coma...
``` Rare AMS Hypothermia Decreased cardiac output Increase vascular permeability increase water retention ```
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Treatment for myxedema coma..
Passive rewarming Cardiac monitoring Intubation for respiratory failure IV levothyroxine- 500 mpg loading dose then 50-100 msg daily after Alternative medication IV liothyronine 10-20 mcg loading dose 10 mpg Q 4-6 hours x 48 hours risk for arrhythmias ``` D5W infusion Monitor Na Avoid fluid overload For adrenal insufficiency IV hydrocortisone 100mg loading then 25-50 mg Q8 after May need vasopressors ```
113
Examples of primary hypothyroidism...
Autoimmune, thyroidectomy, RAI
114
Examples of secondary hypothyroidism...
Medication induced, pituitary adenoma, adrenal insufficiency
115
Major causes of hyperthyroid...
Graves' disease (60-80% have one of these first three) Toxic multi nodular goiter Toxic adenoma
116
Classic clinical manifestations of hyperthyroidism...
``` Nervousness Heat intolerance Anxiety Irritability Weight loss Frequent BMs Palpitations Fever Resting tremor hyperreflexia tachycardia/afib exophthalmos ```
117
Lab data for hyperthyroidism...
``` TSH decreased T4 normal or increased T3 increased Increased thyroid resin uptake elevated ESR, CRP Anemia Leukocytosis Hypercalcemia ```
118
Pharmacologic therapy for hyperthyroidism...
Beta blockers for symptoms -Propranolol most common Thioureas: -Methimazole (preferred)- block T3, T4 production -Propylthiouracil -Often used in conjunction with Iodine 131 therapy Repeat thyroid function in 6-8 weeks Titration is based on FT4 levels Recurrence with discontinuance of medication Ineffective with thyroiditis Risk for agranulocytosis/pancytopenia- monitor CBC
119
Nonpharmacologic therapy for hyperthyroidism...
Thyroidectomy- typical treatment for graves disease | Need to be euthyroid prep using medication
120
What is amiodarone thyrotoxicosis...
Can cause hypo from decrease T3 production But more commonly hyper direct toxic effect on the thyroid follicular cells which results in destructive thyroiditis. Enhanced thyroid production Must be monitored closely
121
How do you treat amiodarone thyrotoxicosis...
Propranolol I-131 Have cardiologist involved
122
Diagnostic essentials of thyroid storm...
Marked delirium Fever SVT
123
Management of thyroid storm...
Methimazole- give at higher doses with sodium iodide 1 hour after Propranolol Hydrocortisone ``` Supportive measures antipyretics avoid stimulation cardiac monitoring fluid repletion avoid ASA ```
124
Diagnostic data for hyperthyroidism...
Radioiodine uptake scanning (Hcg first) Thyroid US Orbital CT/MRI
125
What is radioactive iodine therapy.
Progressive destruction of thyroid cells until they are euthyroid Used in conjunction with propranolol and methimazole Check Hcg Smoking cessation is essential I-131 is used
126
Radioactive iodine is contraindicated with...
Graves opthalmopathy.
127
Radioactive iodine therapy causes a risk for...
hyperparathyroidism
128
What labs should be monitored with radioactive iodine therapy...
TSH, FT4, Ca levels
129
Complications of thyroidectomy
Recurrent laryngeal nerve damage- vocal cord paralysis | Hypoparathyroid
130
What is the HPA axis...
Hypothalamic-Pituitary Adrenal Axis
131
What is the most common etiology of cushing syndrome..
Occurs secondary to an excess of circulating cortisol, either endogenous or exogenous from glucocorticoid. ACTH hyper secretion (endogenous) Benign pituitary adenoma Exogenous glucocorticoid production More prevalent in females
132
Most common clinical manifestations of cushing syndrome...
Due to gluconeogenesis and glycolysis ``` Weight gain Glucose intolerance Moon face buffalo hump hirsutism depression Diastolic hypertension ``` Fatigue Slow wound healing Hypercoagulable state Hypokalemia Hypernatremia
133
General labs for cushing syndrome...
``` Impaired glucose tolerance Hyperglycemia Glycosuria Leukocytosis Hypokalemia Hypernatremia ```
134
What is the DEX suppression test?
Get 1 mg of dexamethasone at 11 PM | Colect serum cortisol level at 8 AM the next morning because that is when cortisol levels should peak
135
When do you use the DEX suppression test?
For screening for Cushings syndrome or Hypercortisolism
136
How do you interpret the results of the DEX test...
"negative predictive"- these findings exclude cushings syndrome Under 2 mpg/dL HPLC assay this is diagnostic that they DO NOT have cushings
137
How is a 24 hours urine utilized and interpreted in cushings syndrome..
This is used as a confirmatory test Abnormally high 24 hour urine free cortisol level and creatinine confirms Hypercortisolism Typically 3 x upper limit of normal for lab
138
When is imaging appropriate in cushings syndrome...
Once the DEX suppression, 24 hour urine and ACTH testing is complete Then you can get Pituitary MRI, Adrenal CT, or Chest/Abd/Pelvis CT- these are used if tumor is suspected
139
What are the principles of post op surgical cushings syndrome...
Primary treatment intervention for tumor related cushing syndrome -Trans-sphenoidal resection is the gold standard ``` Post-op: Glucocorticoid replacement Glucose management DVT prophylaxis Monitor for adrenal insufficiency ```
140
What is the function of the HPA axis
When the body experiences stress or the circadian rhythm, neurotransmitters work to produce cortisol. The hypothalamus triggers the release of corticotropin releasing hormone which then acts on the anterior pituitary and leads to the ACTH release from the anterior pituitary which works on the adrenal gland to release cortisol. Also any synthetic glucocorticoids that the patient is receiving will also stimulate this cortisol production and release. If inflammation in the body occurs, this provides negative feedback to the neurotransmitters to the hypothalamus to produce less cortisol.
141
What are some false positives for the DEX suppression test?
Anti seizure medications Estrogen therapy pseudo-bushings state (CRF, Alcoholism)
142
What are the principles for medical management in cushings syndrome...
These are utilized by patients who are awaiting surgical intervention or it is contraindicated Spironolactone- manage hypokalemia Dihydrop CCB- manage HTN Ketoconazole/metyrapone- adrenal enzyme inhibitors so they inhibit synthesis or cortisol in the adrenal cortex- monitor LFTs Cabergoline- dopamine agonist- targets pituitary- monitor free cortisol Monitor K, Cr, NA, CBC Assess for DM, Osteoporosis wean and DC glucocorticoids
143
What physical exam finding can help you to determine pituitary involvement?
Cardinal gazes 3rd cranial nerve palsy
144
Pathophysiology of ADH secretion
Osmoreceptor located in the hypothalamus which are very sensitive to the concentration of sodium and osmolarity. Can be stimulatory or inhibitory to increase or decrease ADH production. Stretch receptors in the carotid sinus, atria and large veins. They can be stimulatory for ADH secretion with decreased volume and afferent activity. Inhibitory for increased volume and afferent activity. Once the stretch or osmo receptors are stimulated the posterior pituitary will secrete ADH by acting on the synthesis. Once ADH is secreted it will result in increased water reabsorption. Water reabsorption is passive by increasing permeability of the renal collecting ducts.
145
Difference b/t DI and SIADH physiologically
DI you have decreased ADH secretion which leads to large volume of dilute urine SIADH you have increased ADH secretion which leads to decreased urine volume and very concentrated urine
146
Types of DI
Neurogenic (destruction of posterior pituitary) | Nephrogenic (Renal tubular defect leading to decreased ADH sensitivity)
147
Common causes of DI
Central: Tumors Surgery Trauma Renal: Renal diseases (genetics) Lithium ADH unresponsive kidney
148
Clinical manifestations of DI
``` may be asymptomatic Or Extreme thirst Polydipsia (2-20 L) Polyuria (2-20L/24hour) Urinary frequency Nocturia Somnolence s/s dehydration- hypotension, tachycardia, poor skin turgor ```
149
Common labs for DI
``` 24 hour urine: Volume osmolarity < 300 Ur Creatinine Specific gravity < 1.010 ``` ``` Hyperuricemia Hypernatremia Hypokalemia Hypercalcemia Serum Osmo > 290 ```
150
Diagnostic findings for DI
MRI of hypothalamus and pituitary to look for neurologic abnormalities
151
Vasopressin challenge in DI, How do you test?
Administration of DDAVP intranasal or IV/SubQ Urine volume/Osmo measured 12 h before and 12 h after administration Assess serum Na (don't want to reduce too quickly)
152
Vasopressin challenge in DI, How do you interpret?
Central DI: Rapid decrease in thirst and polyuria symptoms after administration and you will have a normalizing serum Na Nephrogenic DI: clinically unchanged For marginal improvement: double the dose and reassess
153
Central DI treatment first line therapy
DDAVP for the goal of reducing UOP Can be given intranasal, PO, SubQ, IV PO has less efficacy so requires larger dose Assess Serum Na!!!
154
Central DI medication options
Chlorpropamide- second line choice. Enhances renal response to ADH Thiazide in combo with low sodium diet- more common with nephrogenic DI
155
Central DI monitoring
Monitor serum Na frequently initially to prevent sodium decreasing too quickly
156
Nephrogenic DI treatment first line therapy
Thiazide diuretics and NSAIDs (HCTZ + Indomethacin) Induce a mild hypovolemia. increase proximal sodium and reabsorption which leads to decreased H2O delivery to collecting ducts
157
Nephrogenic DI treatment with lithium toxicity
Amiloride (midamor) (blocks lithium via the sodium channels in the kidneys) Monitor for hyperkalemia and lithium levels frequently
158
Nephrogenic DI monitoring
``` Glucose BUN/Cr K+ Na Ca Plasma and urine osmolarity ```
159
General management of DI with IVF, selection of IVF and monitoring
-If patient unable to take in PO then IVF is indicated. -For hypovolemic shock give saline until perfusion is restored -0.45% Na or D5W with half the FWD given in the first 12-24 h. Monitor serum Na reduction, should not exceed 1-2 mEq/L/h
160
How to calculate free water deficit
FWD= 0.4 x body weight (kg) x [(serum Na/140)-1]
161
Pathophysiology of Adrenal insufficiency
A complete loss of adrenal cortices (Primary) Loss of glucocorticoid and mineralacoritcoid secretion Arises when cortisol levels are not sufficient to meet the needs of the body Cortisol helps to maintain vascular tone, hepatic gluconeogenesis and maintaining glycogen
162
Common causes of AI
Destruction from autoimmune disease (most common) Metastatic disease Deposition diseases: hemochromatosis, amyloidosis, sarcoidosis Congenital adrenal hyperplasia (2nd most common cause)Bilateral hemorrhage Infection Drug induced: ketoconazole, etomidate, Rifampin, anticonvulsants
163
Common causes of acute adrenal crisis
``` Stress Abrupt ACH withdrawal Adrenalectomy Pituitary destruction Adrenal injury Etomidate administration ```
164
Clinical manifestations of Acute AI
``` Acute worsening of the chronic manifestations Hypotension Shock Hypoglycemia Profound dehydration ```
165
Clinical manifestations of chronic AI
``` Fatigue Increased skin pigmentation Weakness weight loss N/V Anorexia Pain Postural hypotension Anxiety Irritability ```
166
General labs for AI
``` Hyponatremia Hyperkalemia Hypoglycemia Elevated ESR Hypercalcemia Elevated BUN Metabolic acidosis Neutropenia Lymphocytosis Eosinophilia ``` Check cultures to look for infection
167
Imaging for AI
Adrenal CT to look for enlarged glands
168
When to utilize cortisol, serum ACTH, Cosyntropin stim test
When you suspect chronic AI not to be used in acute scenarios
169
How to interpret results of cortisol, serum ACTH, Cosyntropin stim test
AM cortisol < 3 ACTH > 200 Or cortisol levels that fails to rise above 20 with the cosyntropin stim test Stongly suggestive of chronic primary adrenal insufficiency
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Outpatient management of AI
Glucocorticoids - Hydrocortisone 10-15 mg BID - Prednisone 2-4 mg AM, 1-2 mg PM Mineralocorticoids -Fludrocortisone 0.05-0.2 mg PO daily or every other day
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How to diagnose acute adrenal crisis
``` Abdominal s/s hypotension shock stupor loss of consciousness ```
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How to manage acute adrenal crisis
Endocrinology consultation- nephrology can also be used STAT cortisol, ACTH, Chem, Cultures Hydrocortisone (100-300 mg) + IVF without delay Continue hydrocortisone 50-100 IV Q 6 Treat electrolyte disturbances, glucose monitoring ABX- if suspect infection Once stable: Hydrocortisone + Fludrocortisone (once off IV hydrocortisone and it has been tapered)
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Common causes of SIADH
Euvolemic hyponatremia Tumors - small cell lung CA - Prostate - Thymic - Pancreatic - Lymphoma PNA, TB, Lung Abscesses ETOH withdrawal Head injury, vasculitis, SLE, SDH ``` Drugs: Clorpropamide carbamazepine cyclophosphamide vincristine phenothiazines ``` Surgical procedures
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Clinical manifestations of SIADH
Due to hyponatremia ``` Malaise NV HA Decreased UOP edema lethargy decreased DTR Resp arrest seizure coma death ```
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Characteristic lab findings for SIADH
``` Hyponatremia decreased serum osmo < 280 Urine Na >20 Absence of heart, kidney liver disease normal thyroid and adrenal function ```
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Symptomatic management of SIADH
- Fluid restriction 500 ml/dau - Increase Na by 1-2 mEq/L/h then decrease to 0.5 - 1 mEq/h - 3% saline +/- lasix monitor serum and urine Na Q 2-4 h seizure precautions
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Asymptomatic management of SIADH
- Fluid restriction 500-1000 ml/day - NS or 3% - Correct serum Na by 0.5 - 1 mEq/l/h - Demeclocycline can be given if they cannot adhere to fluid restriction -Vasopressin receptor antagonist- Tolvaptan
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Consequences of rapid/over correction of NA
- Cerebral osmotic demyelination - Stripping of the myelin sheath in the mid brain, thalamus, basal nuclei and cerebellum - Catastrophic and irreversible - Can be delayed 2-6 days after overcorrection
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What is the cosyntropin stimulation test?
Check pre-test AM cortisol Then administer 0.25 mg IV cosyntropin Second cortisol level 30-60 minutes after administration Normal response should be a rise above 20 mg/dL of cortisol Hydrocortisone should be held 8 h prior to testing.
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How do you measure the effectiveness of glucocorticoid therapy in Adrenal insufficiency
Clinically improved, normal WBC, absence of s/s of cushings
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How do you measure effectiveness of mineralocorticoid therapy for AI?
Orthostatic BP measurements NA, K ratio
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Pheochromocytoma causes
Rare Tumor that arises from the adrenal medulla- increased catecholamine secretion Triggered by stress, exercise, trauma, vaginal delivery, anesthesia, IV contrast
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Pheochromocytoma hallmark clinical presentation
-Presents 3rd-5th decade of life - 5 Ps: (know for exam) Pain- HA Perspiration-Excessive Palpitations- Tachyarrhythmias Pressure- HTN Pallor- initially- flushing late Feeling of doom lower chest/abdominal pain multisystem crisis: ARDS, AKI, Acute HF, hepatic failure
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Pheochromocytoma differential diagnosis
``` Migraine HA Essential labile HTN Thyrotoxicosis Anxiety/panic attacks Angina Gastritis Hypoglycemia Amphetamine or cocaine use ```
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Pheochromocytoma labs
``` Hyperglycemia Proteinuria Glycosuria Leukocytosis Thyroid normal ```
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Pheochromocytoma diagnostics
CT/MRI abdomen- tumor | Whole body Iodine-IMBG scan- lights up the adrenal tumor
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Principles of medical management of pheochromocytoma
Alpha blockers is the 1st line therapy (phenoxybenzamine, Doxazosin) Beta blockers (propranolol, metoprolol) CCB (Nifedipine) For HTN crisis: Nicardipine, Nipride, phentolamine For cardiac arrhythmias (Lidocaine, esmolol)
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Confirmatory labs and diagnostics
Plasma free metanephrines initially (screening) - normal levels exclude -Must be drawn in supine position in a quiet dark room 24 hour urine testing- confirmatory Fractionated metanephrines, Fractionated and free catecholamines False positives occur in 10-20% of patients Review table 26-13 in CMDT
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Surgical management for pheochromocytoma
Laparoscopic resection is the treatment of choice After 4-7 days of BP control IV nicardipine or Nipride intra-op
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Complications of surgical management of pheochromocytoma
Hypotension secondary to catecholamine depletion Cardiac arrhythmias Adrenal insufficiency Adrenal hemorrhage
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Difference between DKA and HHS population
DKA are Type 1 DM or very obese type 2 DM | HHS are Type 2 DM patients. Most likely in elderly patients with DM
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DKA clinical manifestations
Elevated BG, Acidosis, ketosis Polydipsia, Lethargy, fatigue, Acute confusion Kussmaul breathing Confusion, Nausea, Vomiting, Abdominal pain Polyuria, glycosuria, ketonuria Muscle wasting
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HHS clinical manifestations
``` Polyuria Weakness Lethargy/confusion Hypotension Tachycardia Profound dehydration Poor skin turgor ```
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Difference between DKA and HHS lab abnormalities
HHS has no or small ketones and are not acidotic Serum bicarbonate is normal They have a high serum osmolality and usually BG levels are higher DKA are positive for ketones, have an anion gap. Are acidotic and low serum bicarbonate
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DKA management
``` Fluid replacement (1L/hr NS) -Fluid determination by corrected Na -Once BG is 200 then you switch the D51/2NS at 150-250 / hr Replace potassium -Check renal function -replace per hospital protocol Insulin -IV infusion -0.1 u/kg as a bolus -0.1 u/kg/hour infusion -should drop by 50-75 mg/dL/hour if not double insulin -Once BG is 200 reduce the insulin infusion. Keep BG between 150-200 until anion gap closes Assess the need for Bicarb -only use for pH<6.9 -This is controversial ```
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HHS managment
``` IV fluid replacement- very important, may never require insulin. -determined by volume status -start with NS -Use 1/2 NS for high or normal serum NA -Use D51/2 once serum BG 300 Correct hyperosmolar state Insulin -0.1 u/kg as bolus -0.1 u/kg/hr continuous Replace potassium ```
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When do you convert an insulin gtt to SQ
In order to convert to SQ insulin in DKA patients should: Be eating Alert BG < 200 Resolution of acidosis (AG < 12, HCO3 > 15) In order to convert to SQ insulin in HHS: Be eating Alert BG < 250
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Causes of hypoglycemia
``` Cortisol deficiency Tumors- pancreatic B cell Certain medications -BB can mask s/s of hypoglycemia DM medications Accidental/Malice overdose insulin ```
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Clinical manifestations for hypoglycemia
``` Neuroglycopenic effects: Confusion Fatigue Seizures Focal neuro deficits Adrenergic effects: Palpitations Tachycardia Tremors Anxiety Cholinergic effects: Diaphoresis Hunger Paresthesia ```
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Hypoglycemia lab/diagnostics
``` Check plasma glucose level Insulin C-peptide Sulfonylurea Beta-hydroxybutyrate Proinsulin insulin antibody Cortisol level Growth hormone level CT scan- tumors ```
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Hypoglycemia treatment options
If alert with gag reflex: 16 grams glucose tabs or 15 grams carbs- juice/candy recheck in 15 minutes ``` Decreased LOC: D50 IV 25-50 grams Glucagon 1 mg IM or SQ D50 or D10 infusion -Q1 h BG, increase infusion by 10 until improved ``` All patients: DC offending meds monitor closely
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DKA labs/diagnostics
``` Elevated BG Hyperkalemia progressing to Hypokalemia Anion gap Need to look at corrected sodium ABG- Decreased Ph Low bicarbonate Elevated WBC check CXR and EKG ```
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Serum osmolality calculation
2(Na) + Glucose/18
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Anion gap
Na-(HCO3 + Cl)
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Corrected serum Na
Na + [0.016 (measured glucose-100]
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Risk factors for hypoglycemia
``` incorrect insulin dosing Fasting Exercise ETOH Renal dysfunction GI illness Age Prior episodes of hypoglycemia Increased insulin sensitivity ```
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How to calculate free water deficit
0.4 x body weight x [(serum Na/140)- 1]
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For every 1 L of free water deficit there is a...
3-5 mEq increase in sodium